The Brainstem Blueprint: What Neuroscience Reveals About Your Neck's Role in Headache, Jaw Pain, and Dizziness

What two significant 2025 research papers have now mapped in detail is what clinicians working in the craniocervical space have long observed in practice: that the upper cervical spine has direct anatomical connections to the brain regions responsible for head pain, facial and jaw sensation, and spatial orientation. Not metaphorical connections. Not statistical correlations. Documented neuroanatomical pathways — now the subject of a combined 83-study scoping review and a comprehensive perspective paper from an international team that includes some of the most published researchers in the cervical dizziness field.

This post goes deeper into the neuroscience than our overview article. If you want the clinical picture first, start with The Neck, the Jaw, and the Headache and return here when you want the anatomy behind it.

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The Two Brainstem Regions at the Centre of This

The brainstem — the stalk of neural tissue connecting the spinal cord to the brain — is where the cervical spine's influence on the head is mediated. Two distinct regions within it are relevant here, and understanding what each one does is the key to understanding why cervical dysfunction can simultaneously produce headache, jaw symptoms, and dizziness.

The trigeminocervical nucleus (TCN) — a region extending from the medulla down through the upper cervical spinal cord (C1–C3) — is where sensory signals from the face, jaw, teeth, meninges, and orofacial structures converge with sensory signals from the upper cervical spine. This convergence produces the referred pain phenomenon: nociceptive input from one region activates neurons that the brain associates with the other, producing pain that appears to come from somewhere it does not originate.

The vestibular nuclei and cerebellum — lower brainstem structures responsible for processing balance, spatial orientation, and head position — receive their input not just from the inner ear but from the cervical spine itself. The density of proprioceptive receptors in the upper cervical musculature — particularly the suboccipital muscles — is among the highest in the human body. That proprioceptive signal is a continuous, real-time feed of information about head position, and the brainstem uses it alongside vestibular and visual signals to maintain spatial orientation.

When the cervical spine is dysfunctional, both of these brainstem regions are affected. The clinical consequences are not two separate problems — they are two outputs of the same disturbed input system.

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Part 1: The TCN — A 2025 Mapping of 83 Studies

A 2025 scoping review by Pankrath and colleagues — published in the Journal of Oral & Facial Pain and Headache — is the most systematic mapping of the TCN's connections to date. [1] Drawing on six major databases and screening 1658 records, the review included 83 studies examining the anatomical, histological, biochemical, electrophysiological, and clinical evidence for connections between the orofacial, cranial, and cervical regions through the TCN.

The structural anatomy, briefly: the TCN extends from the medulla (pars oralis, pars interpolaris) down through the pars caudalis to the upper cervical dorsal horn at C1–C2. It is subdivided into functional zones. The transition between the interpolaris and caudalis (Vi/Vc) was the most studied region (62.6% of studies), followed by the upper cervical cord at C1/C2 (20.5%). These zones receive input from the teeth, TMJ, masseter, facial skin, whiskerpad (in animal models), and the supratentorial dura — converging with upper cervical afferents from C1, C2, and C3.

The key finding: of the 83 studies, 71 (85%) identified the orofacial/cranial-to-cervical direction as the predominant or exclusively studied direction of the connection. Five studies (6%) identified the cervical-to-orofacial direction, and five (6%) documented bidirectional activity.

This directional finding requires careful interpretation. The authors are explicit about this: the predominant studied direction reflects what researchers chose to investigate — they typically applied a stimulus to the jaw, face, or dura and measured the response in the cervical cord, because that was the direction of scientific interest in these mostly pain neuroscience and dental research laboratories. The predominance of orofacial-to-cervical studies does not mean that direction is clinically more important. The authors' conclusion is clear: the connection is bidirectional. Stimuli from either the orofacial/cranial region or the cervical region can activate nociceptive neurons in the other territory. For clinicians, both directions are relevant.

The TMJ was the most studied single orofacial structure, with 12 studies documenting its connections to C1–C3 via the TCN. This places the jaw firmly within the upper cervical clinical picture — not as a separate system requiring a separate specialist, but as a structure whose nociception and the cervical spine's nociception share the same brainstem relay.

The clinical implication the authors state explicitly: assessment and management of patients with orofacial pain, headache, or cervical pain should consider all three regions together. The TCN is the anatomical reason why.

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Part 2: The Cerebellum — The Dizziness Side of the Same System

The vestibular connection to the cervical spine runs through a different pathway but tells a related story. A 2025 perspective paper by De Hertogh and colleagues — co-authored by Sue Reid, whose randomised trial of manual therapy for cervicogenic dizziness remains one of the strongest pieces of clinical evidence in the field — provides the most current account of how cervical proprioception feeds into the balance system. [2]

The pathway is this: cervical proprioceptive afferents — from muscle spindles, Golgi tendon organs, and joint mechanoreceptors in the upper cervical musculature — travel to the central cervical nucleus. From there, they project to the cerebellum and the reticular formation.

This matters because the cerebellum is not simply a relay station. It is an active comparator — a system that receives vestibular input from the inner ear, proprioceptive input from the cervical spine, and visual input from the eyes, and continuously monitors them for consistency. When all three inputs agree, spatial orientation is stable. When one input conflicts with the others, the cerebellum detects the mismatch and initiates compensatory responses.

The significance of the cervical-to-cerebellar pathway is demonstrated by what happens when it is removed. Unilateral transection of C1–C3 dorsal roots in animals produces effects indistinguishable from a unilateral labyrinthectomy — nystagmus, ataxia, and a profound sense of tilting, without any damage to the inner ear at all. The cerebellum cannot distinguish between a disrupted vestibular signal and a disrupted cervical proprioceptive signal: both produce the same sensorimotor mismatch.

De Hertogh and colleagues also document that the cerebellum can compensate for vestibular loss using cervical proprioception — an animal model shows that following contralateral labyrinthectomy, monkeys can perform head movements as precisely as healthy controls, provided their cervical proprioceptors are intact. The cervical spine is not a passive contributor to balance; it is an active redundant channel that the cerebellum relies upon.

When upper cervical dysfunction — joint restriction, suboccipital myofascial tension, post-whiplash sensitisation — degrades the quality of cervical proprioceptive signals, the cerebellum receives inaccurate information from one of its three primary input channels. The result is sensorimotor mismatch: the brain's representation of head position diverges from what the vestibular and visual systems are reporting. This is experienced as dizziness, unsteadiness, visual motion sensitivity, and a sense of spatial unreliability.

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Part 3: Central Maladaptation — When the Problem Becomes Self-Sustaining

De Hertogh and colleagues introduce an important dimension that the clinical literature on cervicogenic dizziness has not always emphasised: central maladaptation. [2]

In straightforward cervicogenic dizziness, the sensorimotor mismatch is peripheral — it originates from altered cervical proprioceptive input and resolves when the cervical dysfunction is treated. But in persistent cases, the central nervous system's compensatory mechanisms can become maladaptive. Sensory reweighting — the process by which the brain adjusts how much it trusts each input channel — can overcorrect. Visual dependence increases. The vestibular and proprioceptive channels are progressively downweighted. Anxiety and vigilance develop around movements that provoke dizziness, creating a feedback loop that perpetuates symptoms even when the original peripheral source has been partially resolved.

This overlap with Persistent Postural-Perceptual Dizziness (PPPD) explains why some cervicogenic dizziness cases are straightforward — treat the cervical dysfunction, resolve the dizziness — while others require a more graduated approach that addresses both the cervical source and the central reweighting that has developed around it. The sensorimotor retraining component of cervicogenic dizziness management — the gaze stabilisation exercises, head movement tasks, and progressive vestibular challenges — is specifically directed at restoring appropriate sensory weighting, not just at the cervical mechanics.

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Why Both Systems Are Disrupted by the Same Source

The TCN and the vestibulocerebellar system are anatomically proximate in the brainstem and receive their cervical input from the same spinal levels: C1, C2, and C3. This is not a coincidence — it is why the same upper cervical dysfunction can simultaneously produce:

• Head pain and facial or jaw symptoms (via the TCN, where cervical afferents sensitise the trigeminal territory)
• Dizziness and spatial disorientation (via the vestibulocerebellar pathway, where cervical proprioceptive signals corrupt the cerebellar comparator)

And — as documented by the Hack 1995 cadaveric dissection — the suboccipital muscles, whose dysfunction underpins both of these pathways, have a direct physical connection to the cervical dura via the myodural bridge. [3] Tension in the suboccipital musculature loads the dura directly. Since dural nociception is mediated by the trigeminal nerve, this becomes a third route by which upper cervical restriction produces head pain — operating entirely independently of the TCN convergence mechanism.

Three pathways, one anatomical region.

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What This Changes Clinically

For practitioners, this neuroscience changes the question from "which structure is the source?" to "which outputs of this dysfunctional cervical system are we seeing in this patient?"

A patient presenting with unilateral headache, jaw clicking, and dizziness on head movement is not three patients. The upper cervical spine — its joints, its myofascial system, its fascial compartments, and its proprioceptive output — is the common source, mediated through anatomically described brainstem pathways that 2025 research has now mapped with greater precision than at any previous point.

Assessment that stops at the jaw, or stops at the inner ear, or stops at the head, misses the anatomical reality. The clinical assessment that follows the anatomy necessarily includes the upper cervical spine — its joint mechanics, its myofascial status, its proprioceptive output, and its fascial investments.

Treatment directed at the upper cervical system — manual therapy to the joints, fascial work in the suboccipital and posterior cervical compartments, deep cervical flexor rehabilitation, sensorimotor retraining — addresses all three outputs simultaneously, because it addresses their shared source.

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What This Means for You

If you have been told your dizziness is "not an ear problem" and nothing further has been offered, the cervical proprioceptive pathway described in Paper 186 [2] is the mechanism most likely to be relevant to your presentation. Cervicogenic dizziness is mechanistically understood and has a documented evidence base for manual therapy treatment — the same Sue Reid who co-authored this 2025 perspective paper was the lead author on the randomised trial showing significant dizziness reduction at 12 months following cervical manual therapy.

If you have headache and jaw symptoms that coexist, the bidirectional TCN connections documented across 83 studies [1] confirm that treating only the jaw or only the head leaves the network partially unaddressed. Cervical assessment is not supplementary — it is mechanistically indicated.

If your symptoms have persisted despite treatment of the apparent primary site, the central maladaptation dimension described by De Hertogh and colleagues [2] may be relevant. Persistent cervicogenic dizziness and headache can involve central reweighting that requires a graduated sensorimotor rehabilitation approach, not just structural treatment of the cervical source.

If you have all of the above, the brainstem anatomy described in both papers points to the upper cervical spine as the starting point for a comprehensive assessment.

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Want to discuss whether your symptoms fit this picture?

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