Experts describe the multifactorial association between migraine and comorbid psychiatric disease and consider the role of neurogenic inflammation.
Stephen Silberstein, MD; David Dodick, MD; Stewart Tepper, MD; and Peter Goadsby, MBBS
PUBLISHED December 13, 2018
Stephen Silberstein, MD: What about the concept that’s going around that most psychiatric disorders are neuroinflammatory disorders? There’s a case story of someone who had bipolar disease: they gave her a transplant of lymphocytes and her bipolar disorder went away. People are now commenting on the fact that in many disease states the immune reaction is what drives it. If you eliminate the immune reaction, could they make migraine and the psychiatric disorders morbid, with relation to the immune system?
David Dodick, MD: I don’t know the answer to that. It’s probably multifactorial in the way that these genetic variances give rise to 2 different disease states. Neuroinflammation is certainly an emerging and growing field, no doubt. Its role in migraine and psychiatric disease, and its role in many other disease states is really not clear yet.
Stewart Tepper, MD: It behooves us to be thinking, as neurologists, about each of these comorbid conditions, as we reach out with our treatments. It really is important to have a discussion about depression, anxiety, migraine, and peptic ulcer disease because of the issues of using their nonsteroidal anti-inflammatories in the setting of migraine, because some of the medications that we prescribe have adverse effects on the comorbid illnesses—and sometimes you can get a 2-for-1 treatment. If one doesn’t proactively seek out that history, one cannot optimally treat it. It’s so important that it is part of every clinician’s day-to-day interaction with a migraine patient.
Peter Goadsby, MBBS: From a mechanistic point of view, I think the inflammatory story didn’t make much progress in the last 15 years in migraine. When you look at the medicines that were developed to chase inflammatory targets, substance P antagonists, the plasma protein extravasation inhibitors and the TRPV1 antagonists, they all failed in controlled trials. During this discussion, we’re going to be talking about things that have worked. It’s important, when we’re talking about these things that have happened, that we learn a lot by negative things as well; not everything works in migraine. One of the nice things about migraine as a field is we’ve been able to apply biology at several levels to yield information that’s both positive and negative, to increase our understanding. At one level it’s disappointing that those medicines didn’t work. But at another level, it reinforces what we need to work on.
David Dodick, MD: I couldn’t agree more because when you look at this field, we’ve moved away from the vessel as a target. For decades we wanted to constrict the blood vessel because we thought that was important in the biology of this disease. We moved away from that and, as Peter says, into neurogenic inflammation. We chased 2 decades worth of new molecules that didn’t pan out. Now we have much more specific, relevant, and robust targets that are giving rise to therapies that are changing this field forever.