Migraine and Neck Pain: Understanding the Powerful Brain-Spine Connection

From Vascular Theory to Neurological Complexity

Historically, migraines were believed to be caused by dilation of cerebral blood vessels.

This vascular theory has since evolved. Today, migraine is understood as a disorder of sensory processing, involving:

• Cortical spreading depression (CSD)
• Brainstem and hypothalamic dysfunction
• Activation of the trigeminovascular system
• Release of neuropeptides such as calcitonin gene-related peptide (CGRP)
• Central sensitisation and altered pain thresholds

These processes work together to produce not only headache, but also nausea, visual aura, fatigue, and sensitivity to light, sound, and smell (Goadsby et al., 2017).

---

Cortical Spreading Depression (CSD) and Aura

In migraine with aura, a phenomenon known as cortical spreading depression causes a wave of electrical silence across the cortex.

This disrupts normal neuronal activity and is followed by a cascade of inflammation, vasodilation, and CGRP release. CSD likely explains symptoms such as visual changes, tingling, and dizziness preceding the pain phase (Goadsby et al., 2017).

---

The Trigeminocervical Complex (TCC): A Shared Pain Pathway

A critical anatomical structure in migraine pathophysiology is the trigeminocervical complex (TCC) – a region in the upper cervical spinal cord where sensory fibres from the trigeminal nerve (cranial nerve V) and afferent fibres from cervical nerves C1–C3 converge and synapse onto shared second-order neurons (Bartsch & Goadsby, 2003).

This convergence explains:

• Why migraine pain is often felt in the neck, jaw, and occiput, in addition to the head
• How cervical spine dysfunction can trigger or amplify migraine episodes
• Why treatment targeting the neck (e.g., manual therapy or postural correction) can reduce migraine symptoms in some patients

---

C1–C3 Afferents: Driving Input into the Brainstem

The upper cervical afferents from C1–C3 transmit sensory information from joints, muscles, dura mater, and vascular structures in the upper neck.

These fibres project into the spinal trigeminal nucleus, where pain input from the face is also processed. This anatomical and functional overlap means:

• Neck dysfunction (e.g., facet joint irritation, muscle tension, poor proprioception) can activate the TCC
• This input can sensitise brainstem pain-processing regions and initiate migraine pain
• Headache triggers like posture, cervical loading, or whiplash injuries may have a physiological basis in this pathway (Bartsch & Goadsby, 2003; Schwarz et al., 2022)

---

Proprioception and Sensorimotor Disturbance in the Neck

In addition to pain pathways, the sensorimotor system, particularly cervical proprioception, plays a role in dizziness and disequilibrium often reported during migraine.

Impaired afferent input from deep neck flexors and suboccipital muscles can affect reflexive eye and postural control. This may exacerbate migraine symptoms like dizziness, brain fog, and neck tension (Treleaven, 2008).

---

Brainstem Dysfunction and Central Sensitisation

Prior to the onset of pain, imaging studies have shown activation of the periaqueductal gray (PAG), dorsal pons, and hypothalamus.

These regions modulate pain, autonomic function, sleep, and emotion. Their early involvement supports the theory that migraines are initiated by dysregulated sensory processing in the brainstem (Goadsby et al., 2017).

With repeated attacks, central sensitisation can occur, where the nervous system becomes hyper-responsive to sensory input, leading to:

• Allodynia (pain with light touch)
• Photophobia and phonophobia
• Persistent neck pain or tightness
• Greater headache frequency and disability

---

Clinical Implications: Why the Neck Matters

Manual palpation of the upper cervical spine can provoke headache symptoms in migraine patients, particularly at C0–C2 (Schwarz et al., 2022).

A systematic review and meta-analysis found that neck pain is a frequent complaint among patients with migraine, with a pooled prevalence of 77.0% in the migraine group compared to 23.2% in the non-headache control group (Al-Khazali et al., 2022).

For clinicians, this means:

• The neck should be part of a routine migraine assessment
• Sensorimotor retraining (e.g., cervical joint position sense, deep neck flexor endurance) may play a therapeutic role
• Patients with refractory migraine or neck-dominant symptoms should be screened for cervicogenic headache overlap

Simple Breakdown

• A migraine starts in the brain, not just the head.
• A wave of nerve shutdown (cortical spreading depression) can trigger pain and aura symptoms (e.g. vision changes).
• The trigeminal nerve sends pain signals and releases chemicals (like CGRP) that cause swelling in the brain’s blood vessels.
• The top 3 neck nerves (C1–C3) connect to the same brain area as the trigeminal nerve.
• Neck tension or stiffness can trigger or worsen migraines.
• This is why many people get neck pain with their migraines.
• Balance and dizziness issues can also come from poor neck control.
• Repeated migraines can cause the brain to become too sensitive to touch, light, or sound.
• Physiotherapy can help reduce neck input and calm the system.

Migraine isn’t just a head problem, your neck matters too.

---

Conclusion

Migraine is not just a headache—it’s a multisystem neurological disorder involving complex interactions between the brain, brainstem, and cervical spine.

The convergence of afferent input from C1–C3 and the trigeminal system within the TCC forms the anatomical basis for cervicogenic contributions to migraine.

By integrating cervical assessment and treatment, clinicians may offer more effective, holistic care for those living with migraine.