If you suffer from migraines, you've probably been through the medication carousel. Triptans, beta blockers, anticonvulsants, antidepressants, CGRP inhibitors, Botox. Some helped. Some didn't. Some helped for a while and then stopped working.
The reason the medication approach has limits isn't because the medications are bad. It's because medication is treating the downstream effects of migraine — the pain, the inflammation, the vascular changes — without addressing the neurological event that triggers all of it.
Migraine Is Not a Headache
This is the most important thing to understand about migraine: headache is just one symptom of a much larger neurological event.
A migraine episode involves:
- Cortical spreading depression — a wave of electrical activity that slowly moves across the brain's surface, temporarily altering function in each region it passes through
- Trigeminal nucleus activation — the brainstem pain processing center becomes hypersensitive, amplifying normal sensory signals into pain
- Autonomic dysregulation — changes in blood vessel tone, nausea, temperature regulation, and other autonomic functions
- Sensory hypersensitivity — light, sound, smell, and touch all become overwhelming as the brain loses its normal filtering capacity
The headache is just the most noticeable output of this cascade. Many migraine sufferers also experience brain fog, difficulty finding words, visual disturbances, dizziness, fatigue, and mood changes — all of which are neurological symptoms, not pain symptoms.
If migraine is a neurological event, then treating only the pain is like treating only the cough when someone has pneumonia. The cough matters, but it's not the disease. The disease is the neurological cascade that produces the cough — and addressing that cascade is what prevents the next episode.
What Makes a Brain Susceptible to Migraine
Not everyone gets migraines. And the people who do don't get them all the time. So what determines whether a migraine event gets triggered on any given day?
Current neuroscience points to the concept of a migraine threshold — a level of neurological activation above which the brain tips into a migraine state. This threshold varies from person to person (genetics plays a role) and fluctuates day to day based on accumulated neurological "load."
Factors that lower the threshold — making migraine more likely — include:
- Brainstem sensitization — when the trigeminal nucleus is already running "hot" from chronic activation, it takes less stimulation to trigger a full migraine event
- Cervical spine dysfunction — the upper cervical nerves converge with the trigeminal nucleus in the trigeminocervical complex. Cervical dysfunction can directly sensitize the pain processing center
- Vestibular-migraine interaction — vestibular dysfunction increases brainstem activation. This is why many migraine patients also experience dizziness, and why vestibular symptoms often precede or accompany migraine episodes
- Visual processing inefficiency — when the visual system has to work harder than normal (due to oculomotor dysfunction, convergence insufficiency, or processing delays), it increases cortical activation and lowers the migraine threshold
- Autonomic dysregulation — poor autonomic function creates instability in the systems that normally buffer the brain against overactivation
The Neurological Assessment
When we evaluate a migraine patient, we're not just documenting headache frequency and trying the next medication. We're looking for the neurological factors that are lowering their migraine threshold:
Brainstem and Trigeminal Function
We assess brainstem function through specific reflex testing, oculomotor examination, and evaluation of sensory processing patterns. The goal is to determine whether the trigeminal nucleus is chronically sensitized and what's driving that sensitization.
Cervical Contribution
The cervical spine is one of the most underappreciated contributors to migraine. The trigeminocervical complex — where upper cervical proprioceptive fibers converge with trigeminal pain pathways — means that cervical dysfunction can directly amplify headache signaling.
We assess cervical range of motion, segmental mobility, proprioceptive accuracy, and the effect of cervical positioning on symptom reproduction. Many migraine patients have significant cervical contribution that's never been identified because imaging looks normal — and imaging doesn't test function.
Vestibular Processing
Vestibular migraine is one of the most common and most underdiagnosed forms of migraine. Even in patients without prominent dizziness, subtle vestibular dysfunction can increase brainstem activation and lower the migraine threshold. VNG and rotary chair testing can identify vestibular contributions that aren't apparent on clinical examination.
Visual and Oculomotor Function
Photophobia (light sensitivity) is nearly universal in migraine patients. But it's not just about brightness — it's about how efficiently the visual system processes information. Oculomotor dysfunction (poor saccade accuracy, impaired smooth pursuit, convergence insufficiency) forces the visual system to work harder, increasing cortical activation and, in turn, migraine susceptibility.
Infrared eye tracking gives us objective data on visual processing efficiency, often revealing specific deficits that can be addressed through targeted rehabilitation.
Raising the Threshold Through Neurological Rehabilitation
Once we identify which neurological factors are lowering your migraine threshold, treatment targets those specific factors:
- Brainstem desensitization: Specific exercises and stimulation protocols designed to reduce trigeminal nucleus hyperexcitability
- Cervical rehabilitation: Improving cervical proprioception and reducing input from the trigeminocervical complex that's feeding into the pain pathway
- Vestibular rehabilitation: Normalizing vestibular processing to reduce brainstem activation from vestibular mismatch
- Oculomotor training: Improving visual processing efficiency so the visual system requires less cortical activation to function normally
The goal isn't to stop a migraine once it starts — that's what medication does. The goal is to raise your neurological threshold so that migraines trigger less often, or not at all. It's the difference between carrying an umbrella and fixing the roof.
Who This Approach Helps
Neurological rehabilitation for migraine is most effective for patients who:
- Have frequent migraines (more than 4-6 per month) despite medication management
- Experience migraine with prominent non-headache symptoms (dizziness, brain fog, visual disturbances, neck pain)
- Have medication-resistant migraines or can't tolerate medications
- Have migraines that started or worsened after a concussion or neck injury
- Want to reduce their migraine frequency rather than just treating episodes when they occur
This approach isn't a replacement for acute medication — you still need tools to manage a migraine when it happens. But by addressing the neurological factors that lower your threshold, we can often dramatically reduce how often those tools are needed.
Migraines Running Your Life?
If medication alone isn't controlling your migraines, neurological factors may be lowering your threshold. A free consultation call can help determine whether our approach fits your situation.
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