Migraine and the Cervical Two-Step: Going Nowhere Fast

Watson and his colleague are back at their usual corner table, and a bottle of Morgon (yes, Watson’s colleague has ordered) is beckoning. Watson comments on the rich colour of the typically full-bodied Beaujolais wine. Then, swirling his glass, eyebrows slightly raised he asks, “Have you ever noticed how often people say cervical factors can ‘influence’ or ‘modulate’ migraine and then insist they can’t be causal?”

His colleague laughs quietly. “Yes, I’ve heard that a hundred times. ‘Cervical afferents might exacerbate a migraine, but they can’t cause one.’ This has always struck me as a bit convenient, as if acknowledging the neck without admitting its importance.”

“Exactly,” Watson replies. “And it’s more than just convenient, it’s logically inconsistent.”

The Diagnostic Paradox

Watson leans in. “Here’s the core issue. Migraine is classified as a primary headache. By definition this means it has no known structural or identifiable cause.”

“Right,” his colleague nods. “So, when clinicians encounter cervical involvement in a migraine case, they say: ‘Well, it can’t cause the migraine, because migraine is primary.’”

“Which,” Watson replies, “is ‘circular reasoning’. Migraine is defined as idiopathic, i.e., no known cause. So, when something potentially causal shows up, like cervical dysfunction, it’s dismissed not because of the evidence, but because of the classification.”

“Ah,” comes Watson’s colleague, pointing his glass for emphasis. “Migraine is primary; therefore, it has no known cause; therefore, cervical input cannot be causal, because migraine is primary.”

“Precisely” Watson says. “That’s textbook circular reasoning. Or, if you prefer the Latin, ‘petitio principii’, ‘begging the question.’”

When Definitions Become Dogma

Watson’s colleague frowns thoughtfully. “But that’s more than a logical error, it’s a clinical one. If we refuse to investigate potential causal peripheral mechanisms, because of the label we have been given, aren’t we letting the classification become the explanation?”

Watson smiles. “Yes, and that is a classic ‘category error’. We’re confusing a diagnostic category, a naming convention, for a neuroscience understanding. ‘Primary’ doesn’t mean cervical afferents aren’t involved. It just means we haven’t definitively proven a musculoskeletal, noxious cervical afferent cause.”

Watson’s colleague, savouring another sip of the Morgon, confidently replies, “Which is very different from saying one doesn’t exist, especially when there’s growing evidence showing that noxious input from the upper cervical spine can sensitise the trigeminocervical complex, the very core of migraine pathophysiology.”

“And yet, the prevailing model treats this as peripheral trivia. As if cervical input is just background noise, not a potential driver.” explains Watson.

The Danger of Dismissal

Watson leans back. “Here’s where it becomes more than academic. This kind of reasoning prevents meaningful inquiry. If you start with the assumption that cervical involvement can’t be causal, then why would you study it further? Why would manual therapists be involved, trained to assess the upper cervical spine thoroughly?”

Watson’s colleague replies fatalistically, “Therefore, why fund research into it; why include it in diagnostic frameworks or headache management guidelines?”

“Exactly,” Watson says. “And so, a loop is created. The classification discourages exploration, which limits data, which reinforces the original assumption.”

They sit in silence for a moment, letting the weight of the thought settle in… then, “‘Confirmation bias’ in action,” comes Watson’s colleague’s thoughtful reply. “We only see what we expect to see  and we disregard what doesn’t fit.”

Reframing the Cervical Question

Watson refills their glasses. “So where does that leave us? It’s not enough to point out the logical error. We have to offer a better way forward.”

“Agreed,” says his colleague. “Maybe that starts by reframing the question. Not is cervical dysfunction the cause of migraine, rather, can cervical afferents play a causal role in the migraine process?”

Watson nods in agreement, “Yes, the diagnostic classification can then be seen as a guide and not a gatekeeper.”

Watson’s colleague, swirling his wine pensively adds, “And it also invites more nuanced treatment strategies. Because if cervical input can sensitise the TCC in migraine, then maybe assessing and treating the upper cervical spine isn’t just helpful it’s essential.”

Watson raises his glass slightly. “We’ve seen it clinically. Patients whose migraine improves not with medication, but with targeted manual therapy and education, i.e., increased knowledge of musculoskeletal control. Not always of course, but often enough to challenge the paradigm.”

Toward a More Integrated Headache Model

“So,” Watson’s colleague says, leaning forward, “we need a new model. One that accepts that idiopathic doesn’t mean impenetrable. That considers migraine not as a monolith, but as a complex neurobiological phenomenon with multiple potential inputs, including noxious upper cervical afferents.”

“And one that encourages interdisciplinary thinking,” Watson adds. “Neurologists and musculoskeletal clinicians should be collaborating not defending turf.”

Watson’s colleague smiles. “So, the real error isn’t just logical, it’s systemic. It’s a failure of imagination, of humility, of curiosity.”

Watson raises his glass in agreement. “To the end of circular reasoning. And to the beginning of better questions. Here’s to thinking outside the classification.”

They clink glasses again, and for a moment the migraine paradox seems just a little more solvable.