By Drew Hall, D.C., Upper Cervical Chiropractor
Aura is the strangest part of migraine and the part patients describe most vividly. A shimmering arc at the edge of vision that grows over twenty minutes. A blind spot with a jagged, sparkling border. Numbness marching from fingertips to lip. Words that will not assemble.
Roughly a quarter to a third of people with migraine experience it, and understanding what is happening makes it considerably less frightening.
What is physically occurring
Aura is not a vascular event, despite decades of teaching that said otherwise. It is a wave of electrical activity moving across the surface of the brain.
The phenomenon is called cortical spreading depression — a slow wave of intense neuronal and glial depolarization followed by prolonged suppression of activity, first described by Leão in 1944. It travels across the cortex at roughly 3 to 5 millimeters per minute.
That speed is the key to everything you experience. Aura typically develops over 5 to 20 minutes and lasts under an hour because that is how long the wave takes to cross the relevant cortex. Visual aura is most common because the wave usually begins in the occipital lobe, where vision is processed, and the expanding zigzag arc is the wavefront crossing your visual map.
Hadjikhani and colleagues confirmed this directly in humans, using functional MRI during visual aura to demonstrate a spreading wave in the occipital cortex with the characteristics of cortical spreading depression (PNAS 2001;98:4687–4692). This is one of the better-established mechanisms in headache medicine.
The wave also opens the door to the pain. Cortical spreading depression activates the trigeminovascular system — releasing inflammatory mediators that stimulate trigeminal nerve endings in the meninges. That is why aura is so often followed by headache.
Where the upper cervical spine enters
The trigeminal signals generated by that process do not stay in the head. They descend into the brainstem and terminate in the trigeminal nucleus caudalis, which extends downward to the C2 and C3 spinal segments. That region is the trigeminocervical complex, and it receives cervical afferent input in the same place.
The adjacency is functional, not merely anatomical. Two studies by Bartsch and Goadsby in Brain established that dural and cervical inputs share second-order neurons and that each can raise the other’s excitability (2002;125:1496-1509 and 2003;126:1801-1813). Cervical traffic and headache traffic are not separate systems arriving at separate destinations.
This is the honest basis for upper cervical interest in migraine. Not that a misalignment causes aura — it does not, and I want to be unambiguous about that. Cortical spreading depression is a cortical event driven substantially by genetics and neuronal excitability, and no adjustment initiates or prevents it. What the convergence research supports is narrower: sustained afferent input from the upper cervical region can raise the excitability of the same neurons that process migraine pain.
Two mechanisms you will encounter, honestly labeled
Within my profession you will hear about the dentate ligament-cord distortion hypothesis, proposed by Grostic in the Chiropractic Research Journal in 1988. The denticulate ligaments are genuine structures — lateral extensions of pia mater anchoring the spinal cord to the dura. The hypothesis holds that upper cervical misalignment transmits tension through them to the cord. That is a hypothesis, it appeared in a non-MEDLINE-indexed journal, and it has never been validated in controlled research.
You will also encounter Flanagan’s craniocervical “choke point” proposal, concerning obstruction of cerebrospinal fluid and venous drainage at the skull base. It is anatomically thoughtful and it remains a single-author hypothesis without independent validation.
The myodural bridge is different, and it is real. Hack and colleagues described in 1995 the dense fibrous connection between rectus capitis posterior minor and the cervical spinal dura, and a systematic review of 26 anatomical studies confirmed dural connections from rectus capitis posterior minor, rectus capitis posterior major, and obliquus capitis inferior (Spine 2017;42:49–54). The dura is pain-sensitive and trigeminally innervated. That connection is established anatomy; what it means clinically for aura is not.
I would rather label these accurately than let you assume all three carry equal weight.
What to do during an aura
Sit or stop what you are doing — particularly stop driving, since visual aura significantly impairs vision. Move somewhere dim and quiet. Note the time it began; duration is diagnostically useful.
Aura usually resolves on its own within an hour. Treating early, if you use acute medication, is generally more effective than waiting.
When aura requires medical evaluation rather than reassurance
These matter, because some things that look like aura are not.
A first aura after age 50 should be evaluated as a possible transient ischemic attack until proven otherwise, not assumed to be migraine.
Aura that is always on the same side, every time, warrants investigation for a structural cause.
Aura lasting longer than 60 minutes, or aura with weakness, warrants urgent assessment.
Sudden-onset symptoms at full intensity — rather than the characteristic slow spread over minutes — suggest a vascular event. Aura marches; strokes arrive.
Visual loss in one eye only, tested by covering each eye in turn, is retinal or vascular rather than cortical, and needs prompt evaluation.
It is also worth knowing that migraine with aura is associated with a modestly increased risk of ischemic stroke, which is why smoking cessation and blood pressure management matter more in this group.
The upper cervical approach
Testing leads, imaging follows. Specific objective testing determines whether a misalignment exists at all; only then does cone beam CT measure the atlas and axis in three dimensions, and the correction is derived from those numbers.
Delivery is low-force — nothing popped, twisted, or yanked. A correction that holds does not need repeating, so later appointments check retention. Healing takes time: trigeminocervical excitability settles across months, not visits.
The honest limit: upper cervical misalignment has not been proven to cause migraine or migraine aura. The convergence physiology is well documented; the causal claim is not.
This article is for educational purposes and is not medical advice. It does not establish a doctor-patient relationship. A first aura after age 50, aura with weakness, aura lasting over an hour, sudden maximal-intensity symptoms, or visual loss in one eye requires immediate medical evaluation.