Women’s Health: Sleep & Migraine

Written By Laurel Charlesworth

The Neurologist’s Toolkit

  • Sleep Routine:

    • What time do you go to bed, how long does it take to fall asleep?

    • How many times do you wake up in the night? Why? How long to get back asleep?

    • What time do you wake up in the morning? How do you feel?

    Assess function / Daytime symptoms

    Red flags: sleepiness while driving, at work, childcare, etc.

    Behaviours:

    • Weekend sleep vs weekday sleep (vs vacation)

    • Daytime naps

    • Over-the-counter medications / substances

    Screen for disorders:

    • OSA – snoring, fragmentation, waking with a dry mouth or nasal congestion, daytime sleepiness or fatigue.

    • RLS

    • Parasomnias

    • Hypersomnia

    OPTIONAL scales:

    • Pittsburgh Sleep Quality Index (PSQI)

    • Insomnia Severity Index (ISI)

    • Epworth Sleepiness Scale (ESS)

    • IRLS symptom scale

  • Nasal airway: septal deviation, narrow nasal bridge, nasal valve collapse.

    Oral airway: tongue size, Mallampati, palate, jaw, tooth alignment

    Other risk factors:

    • BMI

    • Neck circumference

    • Smaller mid-face (East / Southeast Asian heritage)

    • Respiratory disease (wheeze)

    • ± Neuromuscular weakness*

  • Review general sleep hygiene. Have a go-to clinic handout for simple sleep hygiene measures.
    Refer to sleep medicine when required.

    • Insomnia:

      • Provide resources

      • Refer for CBTi (private or group therapy)

    • OSA/Snoring:

      • Refer for sleep study.

      • Treat nasal congestion.

      • Discuss weight management if appropriate.

      • Refer to non-PAP options, below.

    • RLS:

      • Counsel RE lifestyle factors (coffee, exercise, sleep loss).

      • Review aggravating medications and substances (caffeine, alcohol, SSRIs/SNRIs, anti-histamines, anti-emetics).

      • Address iron status. Iron iron iron iron.

    • Circadian factors:

      • Regularize schedule, keep a consistent wake-up time.

      • Consider light therapy.

      • Counsel regarding jet lag and seasonal time change.

Insomnia

“3P Mode of Insomnia”

Adapted from Spielman et al. Psychiatr Clin North Am. 1987.

  1. Predisposing: traits that lower the threshold for insomnia.

    • Hyperarousal trait: anxiety, rumination, perfectionism, “light sleeper”.

    • Genetic vulnerability: family history of insomnia, evening chronotype.

    • Social factors: female sex, history of trauma or psychiatric illness.

  2. Precipitating: the trigger for acute insomnia.

    • Perimenopause/menopause: vasomotor symptoms, mood change, nocturia.

    • Medical illness or pain. Health related worries.‍ ‍New medication (ex. SSRI/SNRI, beta-blocker, etc).

    • Psychiatric illness or acute stress such as bereavement, major life change.

    • Circadian or environmental disruption: travel, shift work, new sleep environment.

  3. Perpetuating: behaviours and beliefs that keep insomnia going after the trigger resolves.

    • Sleep-wake scheduling: extended time in bed, sleeping in, long or late naps. These lower homeostatic sleep drive, fragment sleep, and destabilize circadian timing.

    • Conditioned arousal: bed becomes linked with wakefulness; clock-watching; anticipatory awakening.

    • Cognitive: worry about sleep, catastrophizing about next-day consequences, orthosomnia (preoccupation with wearable data).

    • Substances: alcohol, caffeine (including in combination analgesics), and hypnotic reliance with rebound insomnia.

Components of CBT-i

    • Time in bed is limited to roughly the patient’s actual sleep time to build sleep pressure and consolidate sleep.
      ex. If the patient goes to bed at 21:00 but feels that they fall asleep at 23:00, their new bedtime is 23:00.

    • The time window is expanded in 15–30 min steps as sleep efficiency improves (typically >85–90%).

    • Caution in: epilepsy, bipolar disorder, patients with falls risk, untreated OSA, safety-critical occupations.

    • Re-links the bed with sleep rather than wakefulness and frustration.

    • Go to bed only when sleepy, on a consistent schedule. No daytime napping.

    • Use the bed only for sleep (and intimacy).

    • Get up if not asleep within about 15–20 min (or if frustrated), and return when sleepy.

    • Targets unhelpful beliefs and worry about sleep that fuel arousal. Examples: “I need 8 hours or tomorrow is ruined.” “If I don’t sleep, I’ll get a migraine.”

    • Techniques: cognitive restructuring, decatastrophizing, reducing clock-watching, etc.

    • Particularly relevant in migraine, where fear of sleep-triggered attacks is common.

    • Reduces physiological and cognitive hyperarousal at bedtime.

    • Options include progressive muscle relaxation, diaphragmatic breathing, guided imagery, body scan, and mindfulness-based techniques.

    • Supporting habits:

      • caffeine and alcohol timing

      • consistent schedule

      • morning light, and less evening light and screens

      • a cool, dark, quiet bedroom

      • regular exercise

    • Education on sleep regulation (sleep drive and circadian rhythm) explains why the other components work.

    • Helpful but ineffective as a stand-alone treatment for chronic insomnia.

CBT-I Resources

Apps: Sleepio, CBTi Coach.

Books: Sink into Sleep: The Insomnia Workbook by Dr Judith Davidson; No More Sleepless Nights by Peter Hauri

Websites:

My Sleep Well
National Sleep Foundation
Canadian Sleep Society

Psychotherapists: Local options, or find a therapist via Canadian CBT-I Map. Many therapists offer virtual CBT-I

OHIP-Covered Group CBTi:

Toronto:

Ottawa: Insomnia Care Clinic (insomniacareclinic.ca)

NOTE: I have no affiliation with any of these clinics. Provided exclusively as a resource for your patients!

Non-PAP OSA Options

CPAP (or BiPAP) remains first-line for moderate-severe or symptomatic OSA. Use these options for PAP intolerance, mild OSA, while awaiting sleep medicine assessment, or as adjuncts. Confirm the diagnosis and severity PSG or HSAT first.

Can initiate or recommend directly:

  • Weight loss: 10-15% loss meaningfully reduces AHI; most effective in patients with obesity.

  • Tirzepatide: Health Canada-approved as of June 2026 for moderate-severe OSA in adults with BMI ≥30 kg/m2, alongside diet and exercise. In trials, AHI fell by about 25/h vs about 5/h on placebo in patients not using PAP. It is not a replacement for PAP in established users. Cost and coverage remain barriers.

  • Positional therapy: for positional OSA (supine AHI ≥2× non-supine). Positional devices such as a bumper belt or positional backpack. We no longer recommend the “tennis-ball technique” (sewing a tennis ball into the back of PJs). Long-term adherence is poor.

  • Alcohol and sedatives: avoid alcohol within 3-4 h of bed; minimize benzodiazepines and opioids.

  • Nasal obstruction: nasal rinse for non-allergic rhinitis; combine with intranasal corticosteroid for allergic rhinitis. This can cause a modest reduction in AHI in some patients, generally only an option for snoring or very mild OSA. This can also improve PAP/MAD comfort and tolerance.

Clinical pearls

  • Recheck sleep testing after any non-PAP intervention or significant weight change. Symptom improvement is not proof of control.

  • Menopausal OSA prevalence approaches that of men, and presentation is often atypical (insomnia, fatigue, morning headache, mood) rather than snoring and witnessed apneas. Screen before attributing symptoms to menopause or insomnia.

  • Menopausal hormone therapy is not an OSA treatment.

  • For CPAP troubleshooting or comfort concerns, have patients contact their vendor first. Many CPAP-related issues can be addressed directly by the vendor without needing an appointment with their sleep physician.

Other options:

  • Mandibular advancement device (MAD): custom and titratable, fitted by a dentist with sleep training.

    • Best for mild-moderate OSA especially if predominantly hypopneas, or PAP intolerance at any severity.

    • Requires adequate dentition and regular follow-up with a sleep dentist. TNJ disease may limit therapy but is not an absolute contraindication.

    • Less effective than PAP on AHI, but comparable outcomes in practice because adherence is often higher.

    • Repeat a sleep study on the device to confirm efficacy (the dentist will usually arrange this).

    • Do not recommend over-the-counter devices, or devices fashioned by a dentist without sleep training as this can cause tooth misalignment and jaw pain.

    • Tonsillectomy for significant tonsillar hypertrophy especially if recurrent tonsillitis. This is less commonly offered for adults.

    • Maxillomandibular advancement (MMA) for selected patients with craniofacial factors.

    • Uvulopalatopharyngoplasty used to be common, but is generally no longer used. Painful surgery with long recovery, with limited overall benefit. Many patients still require PAP in the long-run.

    • Bariatric surgery: for eligible patients with severe obesity.

    • Hypoglossal nerve stimulation (ex. Inspire device) is not Health Canada approved and is not available in Canada.

    • Oropharyngeal (myofunctional) exercises: modest AHI reduction. Reasonable as an add-on or for mild OSA. Patient adherence is often a limiting factor.

    • eXciteOSA: daytime tongue exercise / stimulation for snoring and mild OSA. Oral device to be used 20 min daily x6 weeks followed by weekly thereafter. Health Canada approved, but rarely covered by insurance.

    • Elevate head of the bed: This minimally affects AHI, but can help to a small degree and can be advised to patients with no other options.

Sleep Wearables

    • Inputs:

      • Accelerometry (actigraphy): movement determines sleep vs. wake.

      • Photoplethysmography (PPG): a green LED and photodiode detect changes in blood volume with each pulse.
        From these the device derives:

        • heart rate and HRV (autonomic tone shifts across sleep stages)

        • pulse-derived respiratory rate

      • Red/infrared reflectance: SpO₂ estimate, available on some devices.

      • Skin temperature: especially rings; used for cycle and illness tracking.

    • Algorithms:

      • Proprietary machine-learning models, trained against PSG, combine these signals into sleep/wake and stage estimates.

      • Firmware updates can change outputs, so data aren’t comparable across brands or even across versions of the same device.

      • Algorithm developments consider user interaction in addition to clinical data and reliability.

      • Some devices have regulatory-cleared OSA risk notification features, ex. Apple Watch breathing disturbance notification.

    • “Sleep score”: proprietary composites with no clinical validation.

    Clinically validated, medical grade “wearable” home sleep apnea tests also exist, ie. “Level 4” studies. Interpreted by a physician. Good screening tool for OSA. Validated in several populations including some devices validated in peds and in pregnant patients.

    • Bottom line: the worse the sleep, the worse the reliability.

    • If a patient is concerned about hypoxia on wearable output, order overnight oximetry to check before referring to sleep medicine. Errors are very common due to poor fit, motion, cold extremities, darker skin tones.

    • Sleep vs. wake:

      • Sensitivity for sleep is good; specificity for wake is poor.

      • Devices overestimate total sleep time and underestimate WASO.

    • Stages: agreement with PSG is moderate at best and varies by device. “Deep sleep” and “REM” numbers are the least reliable outputs.

    • Worse performance in the people you see most:

      • insomnia and fragmented sleep

      • OSA

      • older adults

      • arrhythmias, especially AF

      • movement disorders and PLMs

    • Best validated outputs: sleep timing, regularity and resting heart rate trends.

    • Term coined by Baron et al., J Clin Sleep Med 2017: a perfectionistic preoccupation with optimizing sleep-tracker data that worsens sleep.

    • Mechanism:

      • performance anxiety and hyperarousal

      • conditioned monitoring

      • trusting the device over one’s own perception

    • Typical patterns:

      • Spending more time in bed to “earn” a better score.

      • Distress over “low deep sleep.”

      • Resistance to CBTi feedback.

Practical approach when a patient brings wearable data

  • Don’t dismiss it. Ask what prompted the tracking and what worries them.

  • Use it for:

    • sleep timing and regularity (circadian assessment, social jet lag)

    • trends over weeks

    • correlating headache diary entries with irregular sleep or short nights

  • Ignore: staging percentages and single-night scores.

  • Act on red flags: if the device suggests low SpO₂, frequent breathing disturbances, or the patient has OSA symptoms, order proper testing (PSG or overnight oximetry).

  • During CBT-I: a sleep diary is preferred. Consider hiding scores or removing the device, especially if orthosomnia is suspected.

  • One-liner for patients: “Your watch is pretty good at telling when you sleep, not how you sleep.”

  • Encourage patients to trust their own subjective experience of sleep, rather than what the device tells them.

Restless Legs Syndrome: Non-Pharmacologic Management

What’s new in RLS? The 2025 AASM RLS guideline (Winkelman et al. J Clin Sleep Med. 2025) moved iron to the centre of treatment and recommended against dopamine agonists as standard therapy because of augmentation.

Lifestyle measures, removing offending medications and substances, and some simple behavioural changes alone can address many patients’ RLS symptoms without medications. Important non-pharma therapy to consider / advise for your RLS patients.

RLS has significant overlap with migraine, 2x more common in migraineurs than general population. RLS may impact sleep quality and quantity, which can worsen migraine. Consider screening all migraine patients for RLS.

    • Review medications. These are the most common reversible cause.

      • Serotonergic antidepressants (SSRIs, SNRIs, TCAs) and mirtazapine.

      • Sedating antihistamines, including diphenhydramine in OTC sleep aids.

      • Dopamine-blocking anti-emetics (metoclopramide) and antipsychotics.

    • Substances: reduce alcohol, nicotine, and caffeine, especially in the evening.
      Caffeine is one of the biggest provoking factors. I generally recommend a 6 week trial without caffeine!

    • Sleep loss worsens RLS. Address insufficient sleep and comorbid OSA.

    • Screen for secondary causes: iron deficiency, CKD, pregnancy, and peripheral neuropathy as a mimic or contributor.

    • Regular moderate exercise. Avoid vigorous exercise close to bedtime, which can worsen symptoms.

    • Mentally engaging activities in the evening (puzzles, conversation, hobbies). Boredom and immobility worsen symptoms.

    • Leg stretching, massage, or a warm or cool bath before bed.

    • Plan around the circadian peak:

      • Symptoms are worst in the late evening.

      • Schedule long car rides, flights, and theatre outings earlier in the day where possible.

      • Choose aisle seats.

    • Most patients do better with a slightly earlier, consistent bedtime that falls before their symptom peak. Some patients do better with a slightly later bedtime that falls after their symptom peak.

    • Pneumatic compression devices: small RCT evidence. Easy to find online, some websites offer trials.

    • Vibrating pads: evidence for “Relaxis” mat - no longer available in Canada. Un-validated knockoffs available.

    • Tonic motor activation (peroneal nerve stimulation, Nidra device) not available in Canada.

    • Compression stockings: wear during the day to prevent venous stasis.

  • Always check ferritin and TSat (hold iron supplements for 24h before checking).

    The thresholds for treating are higher than for anaemia:

    • Oral iron: ferritin ≤75 µg/L and TSAT <45%

    • IV iron: ferritin ≤100 µg/L and TSAT <45%

    • Brain iron can be low even when serum iron is “normal.”

    Diet (helpful, but rarely enough on its own to reach ferritin targets)

    • Heme iron, best absorbed: red meat, organ meats, shellfish (clams, oysters, mussels), sardines, dark-meat poultry.

    • Non-heme iron: lentils, beans, tofu, pumpkin seeds, spinach, fortified cereals.

    • Pair non-heme sources with vitamin C (citrus, peppers, tomatoes, strawberries) to boost absorption.

    • Cooking in cast iron adds a modest amount of iron.

    • Absorption inhibitors: coffee and tea within about 1 h of an iron-rich meal, calcium and dairy, and PPIs or antacids.

    Making oral iron tolerable

    • Alternate-day dosing: Absorption is equal or better than daily dosing because hepcidin falls between doses, with fewer GI effects.

    • Timing: For best absorption, take on an empty stomach in the morning with vitamin C or orange juice. If nausea is a problem, take with food. Some absorption is lost, but it’s better than stopping.

    • Try different formulations (can direct pt to speak with their pharmacist if you are not familiar with different options).

    • If your patient cannot tolerate oral iron, try a prenatal vitamin instead.

    IV iron:

    • IV iron works faster and bypasses GI intolerance. Consider it when oral iron fails, isn’t tolerated, or absorption is impaired.

    • Ferric carboxymaltose (Ferinject - the agent with the strongest RLS data) was recently approved in Canada. Ferric derisomaltose (Monoferric) are the usual alternatives, with access through infusion clinics.

Laurel Charlesworth