Populations and Risk Factors
- Women affected approximately 3:1 over men; hormonal fluctuations (particularly menstruation) are a significant trigger
- Most cases onset between ages 20 and 40; childhood onset is possible
- Strong familial and genetic predisposition — first-degree relatives have 3-4 times the population risk
- Triggers include emotional stress, hormonal shifts, specific foods (tyramine, caffeine withdrawal, alcohol), sleep disruption, bright light, and noise
Causes and Pathophysiology
Trigeminovascular Mechanism
The central mechanism of migraine is activation of the trigeminovascular system — the network connecting the trigeminal nerve (CN V) to the blood vessels of the meninges.- A triggering event (stress, hormonal shift, sensory overload) activates trigeminal sensory neurons that innervate the dura mater and pial arteries.
- These neurons release calcitonin gene-related peptide (CGRP) — a chemical released by nerve endings that widens blood vessels and triggers inflammation of the vessel walls. This is the source of migraine's throbbing quality: the pulsatile pain tracks the heartbeat because it arises from dilated, inflamed vessels.
- Pain signals travel via the trigeminal nerve to the trigeminal nucleus caudalis in the brainstem, then relay to the thalamus and cortex. The older "vasoconstriction then vasodilation" model is an oversimplification — vasoconstriction occurs during the aura phase (see below), not as the primary cause of pain.
Cortical Spreading Depression (Aura)
In migraine with aura, a slow wave of electrical shutdown spreads across the brain surface — cortical spreading depression (CSD). It moves across the occipital cortex at roughly 3 mm per minute. As the wave crosses visual cortex, it produces the characteristic visual aura: marching scotoma, fortification spectra (zigzag arcs), or photopsia (flashing lights). CSD is not present in migraine without aura, which accounts for approximately 70-75% of cases.Trigeminocervical Nucleus and Cervical Contribution
The trigeminal nucleus caudalis extends down into the upper cervical spinal cord, where it converges with sensory input from C1, C2, and C3 nerve roots. This convergence zone is the trigeminocervical nucleus, and it explains three clinically important things:- Upper cervical dysfunction (suboccipital tension, C1-C3 facet irritation) can sensitize this nucleus and lower the threshold for migraine attacks
- Migraine pain frequently radiates into the neck and suboccipital region because the same nucleus processes both trigeminal and cervical input
- Suboccipital soft tissue treatment and joint mobilization has a measurable prophylactic effect on migraine frequency — by reducing cervical input to the shared nucleus
Central Sensitization
With repeated or prolonged attacks, the trigeminocervical nucleus and thalamus become hyperresponsive to normal inputs — this is central sensitization. It explains why patients develop cutaneous allodynia (scalp hypersensitivity during or after attacks), photophobia, phonophobia, and osmophobia. Allodynia is a clinical sign that central sensitization has taken hold, indicating a more refractory attack state.Signs and Symptoms
Migraine Phases
Migraine is a phased condition, not a single event:| Phase | Timing | Features |
|---|---|---|
| Prodrome | Hours to 2 days before headache | Yawning, food cravings, mood changes, neck stiffness, fatigue, increased thirst |
| Aura | 15-60 min before or during headache (~25-30% of cases) | Visual: marching scotoma, fortification spectra, photopsia. Sensory: unilateral paresthesia spreading from hand to face. Rarely: speech disturbance or motor weakness (hemiplegic migraine) |
| Headache | 4-72 hours | Moderate-to-severe throbbing unilateral pain; nausea/vomiting; photophobia; phonophobia; worsened by routine physical activity |
| Postdrome | Up to 24 hours after resolution | Fatigue, difficulty concentrating, neck stiffness, mood changes ("migraine hangover") |
Diagnostic Criteria (IHS ICHD-3, Simplified)
Migraine without aura (most common): At least 5 attacks lasting 4-72 hours with:- Unilateral location
- Pulsating/throbbing quality
- Moderate or severe intensity
- Worsened by or causing avoidance of routine physical activity
- Plus at least one of: nausea/vomiting; photophobia and phonophobia
Associated Features
- Cutaneous allodynia during or after attacks — from central sensitization
- Cognitive impairment ("brain fog") during and after attacks
- Cervical muscle tension and suboccipital tenderness — both contributing factor and consequence
- Mild autonomic features (conjunctival injection, lacrimation) — milder than cluster headache
Assessment Profile
Subjective Presentation
- Chief complaint: "I get this throbbing pain on one side of my head — it puts me out of commission for a day or two. Light and noise make it way worse, and I usually feel sick to my stomach."
- Pain quality: "It throbs, almost like I can feel my heartbeat in my head. Usually one side. Moving around makes it worse — even walking up stairs."
- Onset: Ask about prodromal warning signs (yawning, cravings, mood shifts, neck stiffness). Ask if they see visual disturbances before the headache — this identifies the aura subtype. Ask about trigger patterns: "Can you predict when one is coming? What seems to set them off?"
- Aggravating factors: Light, sound, strong odors, physical exertion, stress, hormonal changes, caffeine withdrawal, alcohol. Ask specifically about each — patients often have not connected all their triggers.
- Easing factors: "I have to lie down in a dark, quiet room." Cold compress to head or neck. Sleep often resolves the attack. Triptans if prescribed. Ask about prophylactic massage history — "Does regular massage seem to reduce how often you get them?"
- Red flags: Thunderclap onset (peak within 60 seconds) — subarachnoid hemorrhage; headache with fever and neck stiffness — meningitis; new neurological deficits or diplopia; headache after head trauma; first or worst headache of life; headache in immunocompromised patient — emergency referral; do not treat
Observation
- Local inspection: Pallor and diaphoresis during active attack; photophobic behaviors (sunglasses, squinting); temporal artery may be visibly pulsating; patient may avoid light touch to the scalp (allodynia)
- Posture: Guarded, hunched posture during attack; forward head posture and suboccipital tension common between attacks as contributing structural factors
- Gait: No characteristic gait change; patient avoids movement during acute attack
Palpation
- Tone: Suboccipital hypertonicity bilaterally (rectus capitis posterior major/minor, obliquus capitis superior/inferior) — consistently present and the primary MT treatment target. Upper trapezius and SCM tension, frequently bilateral. Temporalis hypertonicity at the temple from trigeminal activation.
- Tenderness: Suboccipital attachments at the occiput (C0-C1 junction) — characteristically tender. Cervical referral path: C1-C3 articular pillars on the symptomatic side — tenderness here that reproduces the patient's head pain pattern confirms cervical contribution via the trigeminocervical nucleus and is a primary treatment target. Trigeminal distribution: tenderness may be present along all three CN V branches on the symptomatic side — supraorbital/forehead (V1), cheek/infraorbital (V2), jaw (V3). Mapping this distribution confirms neurovascular activation and distinguishes active migraine from localized muscle pain. Temporal artery — possible pulsatile tenderness during active migraine; compare bilaterally.
- Temperature: Usually normal. Scalp allodynia (hypersensitivity to light touch) during or following an attack indicates central sensitization — contraindication to scalp work during that phase.
- Tissue quality: Palpable nodules and TrPs in suboccipital muscles, upper trapezius, and SCM. Restricted C0-C2 intersegmental mobility on PA and rotational glide. Reduced fascial mobility through the cervico-cranial region.
Motion Assessment
- AROM: Cervical AROM typically normal or only mildly restricted — this is a key differentiator from cervicogenic headache. Reproduction of headache with cervical movement or sustained end-range positioning suggests cervicogenic component.
- PROM / end-feel: Normal cervical passive range and end-feel. No joint restriction specific to migraine.
- Resisted testing: Normal strength throughout. Any upper extremity neurological finding is a red flag requiring referral.
Special Test Cluster
The SOT cluster for migraine is oriented toward differential diagnosis and red flag exclusion rather than direct confirmation — there is no orthopedic test that confirms migraine.| Test | Positive Finding | Purpose |
|---|---|---|
| VBI Screen (CMTO — red flag) | Dizziness, nystagmus, visual changes, drop attack, dysarthria with sustained cervical extension + rotation | Rule out vertebrobasilar insufficiency before cervical assessment; positive = do not proceed; refer |
| Cervical AROM screen (CMTO) | Normal range supports migraine; headache reproduced by cervical movement suggests cervicogenic component | Differentiate migraine from cervicogenic headache |
| Spurling's Test (CMTO) | Negative — no ipsilateral radicular pain with compression + extension + lateral flexion | Rule out cervical radiculopathy |
| Cranial nerve screen (CN V, VII, IX-XII) (supplementary) | Normal rules out active intracranial pathology; CN V tenderness consistent with trigeminovascular activation | Confirm neurological integrity; exclude intracranial red flags |
| MIDAS Questionnaire (supplementary) | Score >=6 = moderate-to-severe disability | Quantify functional impact; establish treatment baseline |
Migraine vs. other headache types — quick differential reference:
| Type | Pain Quality | Location | Duration | Distinguishing Features |
|---|---|---|---|---|
| Migraine | Throbbing/pulsating | Unilateral (60-70%) | 4-72 hrs | Nausea; photophobia; phonophobia; aura possible; worsened by activity |
| Tension-type | Band-like pressure | Bilateral | 30 min-7 days | No nausea; no photophobia; normal cervical AROM; responds well to MT |
| Cluster | Burning/stabbing | Unilateral periorbital | 15-180 min | Autonomic signs (ptosis, rhinorrhea); male-predominant; attacks in series |
| Cervicogenic | Dull ache | Unilateral, neck-to-head | Variable | Positive cervical AROM/Spurling's; reproduced by neck movement; responds to cervical MT |
Differential Assessment
| Condition | Key Distinguishing Feature |
|---|---|
| Tension-type headache | Bilateral, band-like pressure; no nausea, photophobia, or phonophobia; normal cervical AROM; responds well to MT |
| Cervicogenic headache | Headache provoked by cervical movement; positive Spurling's or restricted cervical AROM; responds to cervical MT |
| Cluster headache | Strictly unilateral periorbital; autonomic features (ptosis, lacrimation, rhinorrhea); 15-180 min duration; male-predominant; MT not a primary intervention |
| Subarachnoid hemorrhage | Thunderclap onset; worst headache of life; fever and neck stiffness possible — emergency referral; do not treat |
CMTO Exam Relevance
- Differentiate migraine from tension headache (throbbing vs. band-like), cluster headache (short duration, autonomic features, male-predominant), and cervicogenic headache (musculoskeletal origin, positive cervical assessment)
- Red flag: Thunderclap headache or "worst headache of life" requires immediate referral to rule out subarachnoid hemorrhage
- Know the four migraine phases: prodrome, aura (present in ~25-30%), headache, postdrome
- Rebound headaches (medication-overuse headache): caused by overuse of analgesics or triptans on 10+ days/month; distinguish from chronic migraine
- Chronic Daily Headache (CDH): headache >=15 days/month for >=3 months; migraine can transform into CDH
- Trigeminovascular activation and CGRP release are central to both migraine and cluster headache pathophysiology
Massage Therapy Considerations
- Primary therapeutic target: suboccipital muscles and C0-C2 segmental mobility — reducing cervical input to the trigeminocervical nucleus is the mechanism for MT's prophylactic effect on migraine frequency
- Sequencing logic: release upper trapezius and SCM first to access the suboccipital layer; suboccipital release precedes cervical mobilization; work superficial to deep, peripheral to central
- Acute attack principle: massage during an acute attack is often contraindicated or requires significant modification — stimulation may worsen photophobia, phonophobia, and nausea; maintain a quiet, low-stimulus environment if treating; scalp work is contraindicated if allodynia is present
- Prophylactic treatment principle: regular inter-attack treatment of suboccipital muscles, upper cervical spine, and cervicothoracic junction reduces migraine frequency, severity, and duration — this is the primary MT value proposition for migraine patients
- Allodynia screening: cutaneous allodynia signals central sensitization; screen before applying scalp or temporal work; if present, avoid those areas entirely
- Medications: triptans cause vasoconstriction (avoid aggressive cervical work on same day); preventive medications (beta-blockers, anticonvulsants, SNRIs, CGRP antibodies) may cause orthostatic hypotension — assist client off table slowly
Treatment Plan Foundation
Clinical Goals
- Reduce suboccipital tone and restore C0-C2 intersegmental mobility
- Deactivate TrPs in suboccipital muscles, upper trapezius, and SCM
- Reduce cervical input to the trigeminocervical nucleus (prophylactic effect)
- Normalize cervicothoracic posture contributing to forward head position
Position
- Supine with head on low pillow or cervical roll for occipital and suboccipital access
- Prone (briefly) or seated for upper trapezius and cervicothoracic work if tolerated
Session Sequence
- General effleurage to upper trapezius and cervical region — assess tissue state; confirm allodynia screening is negative before proceeding to scalp or temporal areas
- Myofascial release to upper trapezius bilaterally — reduce superficial guarding to access deeper layers
- SCM release — sustained compression and gentle stripping; address bilateral tension contributing to forward head posture
- Suboccipital release — sustained gentle compression into rectus capitis posterior major/minor and obliquus capitis superior/inferior at the occipital attachments; this is the primary treatment target; slow, sustained pressure; do not rush
- Temporalis and masseter release — gentle sustained compression; address trigeminal-innervated muscles contributing to headache pattern [omit if allodynia present in temporal region]
- Cervicothoracic junction work — address postural contribution; upper thoracic PA mobilization if restricted
Adjunct Modalities
- Hydrotherapy: Cold compress to forehead, temples, or posterior neck during treatment if the patient reports residual headache symptoms — cold is analgesic and vasoconstrictive. Avoid warm/hot applications to the head and neck during or immediately after an attack. Between attacks, warm towel to the cervicothoracic region before treatment to improve tissue pliability for suboccipital work.
- Joint mobilization: C0-C2 segmental mobilization — gentle PA and rotational glide to restore intersegmental mobility; performed after suboccipital soft tissue release; defer if VBI screen is positive or during an acute attack.
- Remedial exercise (on-table): Gentle active cervical ROM through pain-free range after suboccipital release — assess for improved range and reduced symptom provocation as an outcome measure. Chin tuck (deep cervical flexor activation) to address forward head posture — isometric hold, 5-10 seconds, within tolerance.
Exam Station Notes
- Demonstrate VBI screening before any cervical assessment or mobilization
- Perform allodynia screening (light touch to scalp and temporal region) before applying pressure to these areas
- State clinical reasoning for prophylactic vs. acute approach — the treatment plan above is for inter-attack prophylactic treatment; during an acute attack, most steps would be deferred
- Reassess cervical AROM and suboccipital tenderness post-treatment as outcome measures
Verbal Notes
- Allodynia screening: before touching the scalp or temples, ask: "Is your scalp sensitive to light touch right now?" — if yes, avoid these areas entirely
- Suboccipital work: warn the client that sustained pressure at the base of the skull may produce a temporary headache-like sensation or referral behind the eye — this typically resolves within minutes and indicates the correct structures are being addressed
- Post-treatment: some patients experience mild headache or fatigue for 12-24 hours after deep suboccipital work; this is a normal treatment response; if a full migraine develops post-treatment, reduce intensity next session
Self-Care
- Suboccipital self-release (tennis ball at occiput against wall) — 2 minutes daily for chronic tension
- Identify and track personal triggers (food diary, sleep log, stress patterns) — migraine management is as much about trigger avoidance as treatment
- Regular sleep schedule — sleep disruption is one of the most consistent migraine triggers
Key Takeaways
- Migraine is a neurobiological condition driven by trigeminovascular activation, CGRP release, and neurogenic inflammation — not simply vascular dilation
- CSD is the mechanism of aura; it is present only in migraine with aura (~25-30% of cases)
- The trigeminocervical nucleus explains why suboccipital MT has prophylactic effect and why cervical dysfunction lowers the migraine threshold
- Scalp allodynia signals central sensitization and is a contraindication to scalp work during that attack phase
- Confirm the diagnosis by clinical pattern (IHS criteria) and exclusion of red flags; there is no SOT that confirms migraine
- During an attack, massage requires significant modification or is contraindicated; prophylactic massage between attacks is well-supported