Dr. Ashley Russell, ND

Now that we know what migraines are, it would be helpful to know what causes them, right? Though this condition has been around for millennia, we unfortunately still don’t know the cause of migraines. Doctors still practice what scientists believed to be true for years; migraines are simply due to an expansion of the blood vessels inside your skull, called rebound vasodilation. However, recent research has shown that while this can happen in some migraines, this phenomenon does not appear to be the actual cause of a migraine. In this article we’ll discuss what conventional science now thinks migraines are caused by and more importantly, how from a naturopathic perspective, we view and approach treating migraines.

If you remember from my previous article, there are two main different types of migraines: migraines with auras and migraines without auras. Migraines with auras (classic migraines) are thought to be caused by “cortical spreading depression” in which the neurons (nerves cells) in your brain fire and then brain activity is inhibited.1 Normally, your neurons have to fire or depolarize to transmit messages to other neurons, but in classic migraines, this process goes awry. In addition, a correlation between genetics and migraines with auras has been found.2

On the other hand, the cause of migraines without auras (common migraines) remains unclear. Blood vessel expansion (rebound vasodilation) does occur in these migraines and there are pharmaceuticals, like triptans, that constrict blood vessels, to help ease the pain.3 However, some studies have shown that migraine pain can occur with blood vessel contraction, the complete opposite of what we originally thought the cause was. Or, in some cases, after the migraine pain has subsided, blood vessel dilation can still be occurring.4,5 These new findings strongly suggest that there are other mechanisms at work that cause the actual migraine pain.

A new theory about the cause of common migraines, calcitonin gene-related peptide (CGRP), a type of molecule that causes vasodilation, has been proposed. However, more research is needed since CGRP is also linked to diseases like diabetes, high blood pressure, and arthritis, which are all distinctly different conditions.6,7 As of now, there is not one clear cause for migraine pain in common migraines, which makes it challenging to treat with conventional medicine’s pharmaceutical approach because one drug that works for one person, may not work for another. A more in-depth look at conventional treatments (and their likely side effects) will be discussed in the next article in our series.

How to Treat Migraines

So how do you treat something if the cause is not clear? This is where naturopathic medicine thrives. Naturopathic physicians act like health detectives to figure out the cause of disease for each individual. Since physiologically speaking, there is not a clear underlying cause, we rely on our holistic approach of treating the whole person and seek to promote overall health and wellness. This involves taking a thorough medical history and focusing treatment on basic health foundations such as nutrition, exercise, hydration, stress management, and sleep. I have yet to meet a single person that couldn’t use more support or guidance in at least one of these areas. And in the meantime, while we’re addressing the foundations of health, offering acute non-pharmaceutical remedies, which we’ll discuss in a later article, can be helpful.

When it comes to classic migraines, the genetic link may leave us thinking that nothing can be done. But thanks to the advancement of epigenetics, a growing field of science that looks at altering gene expression without changing the gene itself, genes are more of a suggestion than a permanent fact of life. More and more research shows that we can positively influence our epigenetics by improving our basic health foundations, which may ultimately affect classic migraines.

For any type of migraine, helping our patients monitor and detect underlying triggers is key. If you get a migraine during or after major stressors in your life, then perhaps stress management is something that needs the most attention. Or if you notice after certain meals you get a migraine, perhaps identifying food sensitivities should be our first focus. In my experience, there is usually more than one cause or trigger that needs to be addressed and managed, so we usually take a multifaceted approach. As long as we’re seeing a decrease in the severity, duration, and/or frequency of the migraines, we take those health clues as signs that we’re on the right path to figuring out the cause(s) of migraines for that individual.


_TLB3420Dr. Ashley L. Russell graduated from the Southwest College of Naturopathic Medicine in Arizona where she received training as a primary care physician. She received her B.S. in Applied Ecology from the University of California, Irvine. She is a naturopathic doctor at Serenity Natural Health Center in Frederick, Maryland, with a focus on young women’s health and is also co-founder of LovempoweR, an organization dedicated to changing women’s health care. Dr. Russell is passionate about helping women reclaim their menstrual cycle by alleviating all kinds of menstrual issues including PCOS, infertility, endometriosis, PMS, and painful or irregular periods. In her spare time, Dr. Russell enjoys baking vegan, gluten-free treats, hiking, and spending time with her dog, Honey.


References:

  1. Lauritzen M, Dreier JP, Fabricius M, et al. Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury. J Cereb Blood Flow Metab. 2011;31(1):17-35.
  2. Lea RA, Ovcaric M, Sundholm J, et al. The methylenetetrahydrofolate reductase gene variant C677T influences susceptibility to migraine with aura. BMC Med. 2004;2:3.
  3. Shevel E. The Extracranial Vascular Theory of Migraine. Headache. 2011;51(3):409-417.
  4. Rahmann A, Wienecke T, Hansen JM, et al. Vasoactive intestinal peptide causes marked cephalic vasodilation, but does not induce migraine. Cephalalgia. 2008;28(3):226-236.
  5. Charles A. Advances in the basic and clinical science of migraine. Ann Neurol. 2009;65(5):491-498.
  6. Ho TW, Edvinsson L, Goadsby PJ. CGRP and its receptors provide new insights into migraine pathophysiology. Nat Rev Neurol. 2010;6(10):573-582.
  7. Russell FA, King R, Smillie SJ, et al. Calcitonin gene-related peptide: physiology and pathophysiology. Physiol Rev. 2014;94(4):1099-1142.
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