Neck Pain, Headache & Dizziness

Understanding the cervical spine's role in these apparently disparate presentations requires a brief look at the anatomy that connects them.

---

The Anatomy That Explains Everything

The trigeminal nerve is the primary sensory nerve of the head and face. It carries pain signals from the forehead, the jaw, the sinuses, the teeth, and the meninges. The upper cervical nerves — C1, C2, and C3 — carry pain signals from the suboccipital muscles, the upper cervical joints, the cervical dura, and the posterior scalp.

These two systems converge in a structure in the brainstem called the trigeminocervical nucleus (TCN). At the TCN, trigeminal and upper cervical nociceptive inputs are processed together by the same pool of second-order neurons. When sufficient nociceptive traffic arrives from either direction, the sensitised neurons fire — and the pain is referred into whichever territory the brain has learned to associate with that activation. This is why suboccipital muscle tension can generate frontal headache. Why a cervical facet joint at C2–C3 can refer pain to the orbit. Why jaw pain from the TMJ activates upper cervical pain, and vice versa. [1]

A 2025 scoping review by Pankrath and colleagues synthesised 83 studies on TCN nociceptive integration and established the bidirectional nature of these connections. [2] Orofacial and cranial stimuli can activate cervical neurons; cervical stimuli can activate trigeminal territory neurons. The implication is explicit: clinicians assessing headache, jaw pain, or neck pain should routinely consider all three regions — orofacial, cranial, and cervical — because dysfunction in any one of them can maintain sensitisation in the others.

A 1995 cadaveric study by Hack and colleagues at the University of Maryland added another dimension. [3] They identified a consistent fibrous connective tissue bridge — the myodural bridge — between the rectus capitis posterior minor muscle at the suboccipital region and the posterior dura mater at C1–C2. The bridge was present in all five specimens examined. Its functional significance: contraction of the suboccipital muscles may tension the cervical dura, and persistent dural tethering may inhibit full relaxation of the suboccipital muscles in return — a potentially self-sustaining cycle. This anatomical finding provides a structural basis for why suboccipital dysfunction so consistently accompanies cervicogenic headache, and why manual therapy directed at the suboccipital region can influence dural tension and headache symptoms.

---

Cervicogenic Headache: Spine-Sourced, Often Misdiagnosed

Cervicogenic headache is a headache originating from the cervical spine — a clinical reality that is well established in the literature but frequently missed in practice. The headache is typically unilateral, beginning in the neck or suboccipital region and referring anteriorly to the forehead, orbit, or temple. It is often provoked by sustained neck postures, neck movement, or palpation of the upper cervical joints.

A systematic review by Chaibi and Russell assessed the evidence for manual therapy in cervicogenic headache and found significant reductions in headache frequency, intensity, and disability — with effect sizes comparable to prophylactic medication. [4] A systematic review by Racicki and colleagues reinforced this finding: multimodal manual therapy combined with exercise produces superior outcomes to either approach alone, with deep cervical flexor training as the most evidence-supported exercise modality. [5]

The JOSPT Neck CPG by Blanpied and colleagues groups cervicogenic headache as a recognised neck pain subgroup and recommends combined manual therapy and exercise as the appropriate management pathway — a recommendation consistent across the major systematic reviews in this area. [6] → Cervicogenic Headache

---

Tension-Type Headache: More Musculoskeletal Than Most People Realise

Tension-type headache — the most prevalent headache type worldwide — is conventionally described as a bilateral, pressing or tightening headache without nausea, photophobia, or the pulsating quality of migraine. Its pathophysiology involves both peripheral sensitisation of pericranial myofascial structures and central sensitisation.

A 2023 systematic review by Repiso-Guardeño and colleagues synthesised RCT evidence on physical therapy for TTH across multiple outcome domains. [7] Manual therapy, exercise, and multimodal physiotherapy all demonstrated benefit for pain intensity and headache frequency. An RCT by Espí-López and colleagues using suboccipital soft tissue inhibition and occiput-atlas-axis manipulation found that combined cervico-cranial manual therapy outperformed either approach alone for pain, frequency, pericranial tenderness, and cervical range of motion. [8]

A 2026 chiropractic clinical practice guideline by Trager and colleagues drew on 32 systematic reviews and a Delphi consensus of 57 experts to conclude that spinal manipulation is recommended for cervicogenic headache and recommended within multimodal care for TTH. [9] A 2025 systematic review and meta-analysis by Pensri and colleagues across 77 studies confirmed that cervical musculoskeletal impairments — reduced range of motion, forward head posture, reduced flexor strength and endurance, active trigger points — are measurably present in both migraine and TTH populations. [10]

These findings collectively support what the fascial model predicts: tension-type headache is maintained by pericranial myofascial sensitisation and cervical spine dysfunction, both of which are directly addressable through manual therapy and targeted exercise. → Tension-Type Headache

---

Migraine: A Musculoskeletal Contribution Worth Taking Seriously

The dominant biomedical model of migraine positions it as a neurological disorder — a cortical spreading depression event with a trigeminovascular activation cascade. This is accurate, but it is not the whole picture.

A 2019 systematic review and meta-analysis from Harvard Medical School and Palmer College of Chiropractic by Rist and colleagues pooled five RCTs of spinal manipulation for migraine in 677 participants. [11] The result: spinal manipulation significantly reduced migraine days (Hedges' g = −0.35; 95% CI −0.53, −0.16; p<0.001) and migraine pain intensity. The effect size is modest — this is not a cure — but it is statistically significant and clinically meaningful, particularly in individuals who do not tolerate pharmacological prophylaxis or who have a clear cervical contribution to their migraines.

The cervical contribution to migraine is mediated through the same TCN pathway: upper cervical dysfunction lowers the activation threshold of the trigeminal system, increasing the likelihood and frequency of migraine attacks in susceptible individuals. Addressing the cervical contribution does not eliminate the underlying migraine biology — but in many patients it reduces the frequency and severity of attacks by removing a consistent peripheral sensitising input. → Migraine (Musculoskeletal Contribution)

---

Cervicogenic Dizziness: When the Neck Disrupts Balance

Dizziness originating from the cervical spine — cervicogenic dizziness (CGD) — represents a significant but underappreciated clinical entity. A 2025 perspective article by De Hertogh and colleagues in Frontiers in Neurology documents its prevalence: CGD accounts for five to six percent of presentations in ENT and vestibular practices, up to 40% of patients with neck pain also report dizziness, and 43% of people with chronic neck pain report dizziness as a co-presenting symptom. [12]

The mechanism is sensorimotor mismatch. The cervical spine contains a dense concentration of proprioceptive receptors — muscle spindles and joint mechanoreceptors — that provide positional information to the vestibular nuclei, cerebellum, and cortex. These signals are integrated with vestibular and visual inputs to construct the brain's representation of head position and movement in space. When cervical proprioception is disrupted — by injury, sustained postural loading, fascial restriction, or upper cervical joint dysfunction — the brain receives conflicting positional signals. The perceptual result is dizziness, imbalance, and postural instability that does not resolve with vestibular rehabilitation alone, because the vestibular system itself is not the primary problem. [12]

De Hertogh and colleagues note that the cerebellum processes both vestibular and cervical proprioceptive input simultaneously, and that cervical proprioceptive signals can partially compensate for vestibular loss — and vice versa. This bidirectional compensatory capacity means that chronic CGD often involves a failure of sensory reweighting: the brain has become unable to appropriately down-weight the disrupted cervical signal and up-weight the intact vestibular input, producing a persistent dizziness that endures long after the initial provocating event.

A randomised controlled trial by Reid and colleagues with 12-month follow-up compared SNAGs (sustained natural apophyseal glides) and passive joint mobilisation against placebo for chronic CGD. [13] Both manual therapy groups showed significantly less dizziness frequency, lower Dizziness Handicap Inventory scores, and greater global perceived effect than placebo at 12 months. The response to manual therapy directed at the cervical spine is itself diagnostic — dizziness that improves with cervical treatment is cervicogenic in origin. A systematic review by De Vestel and colleagues added meta-analytic support: moderate quality evidence that manual therapy reduces CGD, with combined manual therapy and exercise showing the strongest effect. [14] → Cervicogenic Dizziness

---

BPPV: Crystals, Not the Cervical Spine — But Worth Distinguishing

Benign paroxysmal positional vertigo is the most common vestibular disorder and the most common cause of dizziness in the general population. It arises from displacement of calcium carbonate crystals (otoconia) from the utricle into the semicircular canals, producing brief, intense episodes of rotational vertigo triggered by head position change.

A Cochrane review by Hilton and Pinder established that the Epley canalith repositioning manoeuvre is significantly more effective than sham or control for resolving BPPV symptoms, with no serious adverse effects. [15] The AAO-HNS clinical practice guideline by Bhattacharyya and colleagues reinforces this: Dix-Hallpike as the diagnostic standard, Epley as first-line treatment, and a recommendation against vestibular suppressant medications, routine imaging, or ancillary vestibular testing. [16]

BPPV is distinguished from cervicogenic dizziness primarily by the character of the symptoms — brief (30–60 second) rotational vertigo triggered by specific head positions, positive Dix-Hallpike — versus the non-rotational, position-sensitive but sustained dizziness of CGD. Correctly distinguishing the two is essential: BPPV responds to repositioning; CGD responds to cervical manual therapy and sensorimotor rehabilitation. Misclassification leads to ineffective management. → BPPV

---

The Fascial Thread Through All

The cervical fascia — studied anatomically by Natale, Stecco, and colleagues in a 2015 cadaveric paper — is a multi-layered, complex system of investing, pretracheal, prevertebral, and visceral fascial compartments that envelop the muscles, viscera, and neurovascular structures of the neck. [17] Restriction or densification within the cervical fascial system can directly influence the mobility and mechanoreceptor function of the upper cervical joints and suboccipital muscles — which, through the myodural bridge and the TCN, influence pain processing in the head and face.

The deep cervical flexors — longus colli and longus capitis — sit within the prevertebral fascial compartment. Their dysfunction in chronic neck pain and cervicogenic headache is well documented, and their rehabilitation through craniocervical flexion exercise (CCFE) training produces measurable improvements in neuromuscular activation, pain, and disability — findings confirmed in a 2009 RCT by Jull and colleagues. [18]

The suboccipital region is not just a location where headaches refer — it is a densely innervated zone where the myodural bridge, the upper cervical joints, and the fascial sleeve of the posterior cervical spine converge with the TCN's nociceptive territory. In our clinical practice, we view this zone as a key interface: changes in fascial tissue quality, joint mobility, and muscle recruitment in the suboccipital region are directly relevant to headache, dizziness, and jaw pain presentations, not just neck pain.

The cervical spine is not simply the structure between the head and the thorax. It is a sensorimotor and nociceptive hub whose dysfunction ripples outward in multiple directions simultaneously — and whose assessment and treatment requires a correspondingly comprehensive approach.

---

What Can You Do Right Now?

Address your neck posture during sustained desk work. Forward head posture progressively loads the upper cervical extensors and suboccipital muscles, increases tension on the cervical dura through the myodural bridge, and sensitises the pericranial myofascial system that contributes to tension-type headache. Screen height, chair support, and frequent postural resets — chin tucks, shoulder rolls, brief standing breaks — all reduce this sustained loading.

Train your deep cervical flexors. The craniocervical flexion exercise — performed lying down, gently nodding the chin toward the chest without lifting the head — targets longus colli and longus capitis, the deep cervical stabilisers most consistently impaired in neck pain and cervicogenic headache. This is not a strength exercise done with effort; it is a precision neuromuscular exercise done with control. Start with five sets of ten gentle nodding movements, building to sustained holds of five to ten seconds as tolerance improves.

Distinguish your dizziness type. Brief, intense spinning with position change that lasts 30 to 60 seconds and resolves completely — that is BPPV and it responds to repositioning manoeuvres, which your clinician can perform. Vague, sustained dizziness or imbalance associated with neck movement, sustained postures, or neck pain — that is more consistent with cervicogenic dizziness and responds to cervical manual therapy and sensorimotor rehabilitation. The two need different management.

Don't wait out a migraine pattern. The evidence that cervical musculoskeletal findings — trigger points, restricted range of motion, forward head posture — contribute to migraine frequency is now substantial. If your migraines are frequent or severe, a cervical spine assessment is a reasonable and evidence-supported component of your management, not an alternative medicine fringe option.

---

Want to understand what's actually driving your neck pain, headaches, or dizziness?

Free 2-Week Rehab Program — request your copy

---