migraine pain

All About Migraines: A Podcast with Angela Stanton

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migraine brain

Migraine has been the focus of my research for over the past decade. Over the years, I had been interviewed many times, some with more and others with less technological success. By this I mean, that sometimes the webcam malfunctions and other times the internet connection on the interviewer’s end fades in and out like one of these two podcasts here.

This time the interview went flawlessly. Everything worked. The interviewer was Dr. Shawn Baker, a surgeon and an athlete, and Zach Bitter, a teacher and ultramarathoner (yeah… 100 miles… oh my). The questions were interesting and covered a very broad range of topics related to migraine, such as diet, medical care, general health, and exercise.

The main concept of an interview like this is to help migraneurs and the general population learn about migraine. The benefit of having expert interviewers like Shawn and Zach is that different segments of the population may also learn. Many of the questions that Shawn asked were questions a doctor would ask to understand migraine better and the questions Zach asked were more appealing to the general population. He also brought up the question of vegetarians, vegans, and migraineurs, as well.

The interview covers how the migraine-brain develops. For example, cyclical vomiting syndrome and IBS are very typical migraine-brain developmental stages, with cyclical vomiting more frequent in pre-puberty boys and IBS in girls. Few doctors realize that these are migraine prodromes. We also discuss some of the medicines most often prescribed for migraine and some of the adverse events that are not recorded as well associated with their use.

Other topics covered include the role of carbohydrates, the genetic setup of the migraine brain, the role of channelopathy in the development of migraine-brain. While migraine as a form of channelopathy is not new, current research is not focusing much on this aspect. This is the very area where much of the benefit may be gained. I view migraine as a channelopathy and discuss this aspect at length. Channelopathy is not preventable or curable, but once its action on the brain is understood, its interference with normal life is preventable. The migraine prevention and treatment protocol that I developed in 2010-2012 and first published first in 2014, and later the second edition book in 2017, is based on preventing the activation of the channelopathic processes that can cause migraine.

Migraine is preventable without the use of any medicines.

Is Your Diet Giving You Migraines?

In case you prefer to watch it on YouTube, the link is here. Please share with migraineurs you know, so they can see that there is hope.

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Migraine Brain as a Survival Advantage: Connecting the Dots with Angela A. Stanton

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migraine radio show

On February 2nd, 2017, Thursday morning at 10 am Central time, I will be on ONE RADIO NETWORK (see schedule here). On this talk show I will present my views about the causes of migraines. The talk show invites advance emailed-in questions to email@oneradionetwork.com, as well as live call-ins during the show at: 888.663.6386. Here is the page where you can listen to the archived recording on the Internet (one hour talk show). If you are in Austin, Texas, you can listen on the radio.

Migraine Brain as a Survival Advantage

For a while we have known that the human body contains approximately 20 thousand genes, although this number seems to be a moving target as technology improves. The latest studies have reduced it to 19 thousand. From the 19 thousand, so far 1254 genes have been associated with migraines. Such a huge number of genes – associated with a condition that plagues nearly 30% of the population – begs for an explanation.

Could it be that migraine at one time in human history provided a survival advantage? A benefit that helped those endowed with this set of genes to survive? The answer to this question must be “yes” because the migraine-brain has survived in the population for so long. It has not been bred out of human populations over the millennia of our evolution. Health conditions disadvantageous for survival normally get deleted from our genome.

The question “why migraine hurts” has a simple answer based on this theory: pluck a group of people with a special adaptation from its natural habitat and place it into a different environment, and what was an advantage suddenly becomes a disadvantage. There are many examples for this in nature.

Greenland Inuit, Canadian Inuit and the Native American populations all have glucose (simple sugar into which all carbohydrates, including fruits and vegetables, grains, nuts, seeds, and some percent of proteins convert) intolerance genes. Fructose (a sweet substance that is approximately half of table sugar; found in fruits, vegetables, and syrups like honey, maple syrup, and of course high fructose corn syrup) can also be problematic. Many of us are born without the necessary enzymes to absorb fructose. The inability to digest sugar can cause diarrhea. In medical parlance, this is called “malabsorption” but the question remains: if so many people are born without the ability to absorb sugar, would that be considered a “malabsorption” or is sugar absorption an adaptation that occurred later in time?  I am not the first one to ask this question.

Now returning to migraine: it is found in at least as large fraction of the population as it is for the inability to absorb sugars, like glucose or fructose. The set of adaptations for the more sensitized brain to danger (that migraineurs today still possess) at one time may have been present in all of our predecessors. Some percent of the ancient population likely never lost this highly sensitized brain adaptation because in the ancient environment it would have provided a survival benefit. However, in our modern life, the highly sensitized brain has become a painful burden, whereas a large percent of the population adapted to modern life, reduced their brain sensitivity and they feel no pain. This is likely similar to how the majority of the population adapted to digest and absorb sugar; only a minority retained their inability to do so, and they still experience painful health conditions as a result.

The cause of migraines is not the pain—the pain is one of many symptoms. Just like medicating children to be able to eat an ice cream makes little sense, so is medicating migraine pain by blocking certain brain functions makes little sense. That is the only thing that the medicines are able to do and they are dished out to migraineurs like candy. Here are three of the most common (and most dangerous) medications given to migraineurs as “preventive” and what they block: Propranolol (blocks cardiac and neuronal voltage-gated sodium channels), Topamax (blocks voltage gated calcium and sodium channels), Amitriptyline (blocks or initiates many channels out of sync, causing major heart damage and sometimes death). Would we put ourselves at these types of risks in order to be able to eat a piece of sugar if we lacked the enzymes to digest them? I think the real problem is the lack of understanding of the true nature of migraines.

Migraines and Salt

Migraine starts with prodromes that are signals of an impending migraine. These prodromes precede a cascade of events that lead to the pain, which starts with the initiation of an alarm status that leads to fight-or-flight from danger. A migraineur can easily be triggered into a migraine by noise, odor, a specific light intensity, and even taste that is above or below the norm. Migraineurs have hyper sensory organ sensitivities (1), more sensory neuronal connections than the norm (2), and this is how perfume can trigger a migraine because that scent is above the norm. A migraineur will start a migraine unless voltage is re-established. Why voltage? Migraineurs use more voltage (3, 4) as a result of the more sensitive sensory organs. Voltage is generated by the sodium/potassium pumps that are located in cell membranes, facilitating voltage differential exchanges between the inside and the outside of the cell. Since more voltage use requires more salt, migraineurs need to consume more salt (sodium chloride). Migraineurs tend to pass more sodium in their urine as a result (5).

The modern Western diet is forever reducing its salt recommendation for the general population, ignoring that a large percent of that population needs more salt than what is recommended. In general, I found that migraineurs need approximately 50% more salt in their diet than non-migraineurs.

Migraines and Sugar

Another factor is sugar. While there is no academic research on migraineurs lacking enzyme to absorb fructose or that they are genetically lacking glucose absorption (although there are many research papers hinting at their possibilities–here is a review of some), it seems, based on the several thousand migraineurs I studied, that migraineurs are either sugar intolerant or are hyper sensitive to sugar—and all forms of carbohydrates. Indeed, migraineurs usually become insulin resistant. It would be quite educational to provide genetic testing to all migraineurs to find out what may drive their intense reaction to carbohydrates. Most migraineurs can completely prevent all migraines by completely avoiding refined carbohydrates, reducing complex carbohydrates to near the low carbs high fat (LCHF) diet levels, and increasing dietary animal fats (not oils).

Myelin is made from fat and cholesterol; it is the white matter in the brain, responsible for insulating the neurons’ axons, the parts that transmit voltage. Since migraineurs transmit voltage more often, their myelin is more likely to get damaged. Glucose seems to aggravate nerves in general in all central nervous systems conditions. The ketogenic (high fat, very low carbohydrate) diet may be ideal for migraineurs since it appears to repair the myelin damage glucose causes. Myelin can be replenished by eating a proper, high in natural fat (not man-made oils) diet and by ensuring that a migraineur retains a healthy insulin response. As expected, migraine is highly correlated with the incidence of insulin resistance (6-8), diabetes mellitus (7), obesity (9), and cardiovascular disease (10).

If migraine were a true disease, dietary changes would not be able to change the brain response in a way that all migraines become preventable and abortable without medications. Since they can be prevented and aborted with the proper migraine-brain diet (an ancient type diet that is void of simple sugars and complex carbohydrates in excess), it follows that migraine is an unintended consequence of the modern Western diet and it is not a disease.

Sources:

  1. Schwedt TJ (2013) Multisensory Integration in Migraine. Curr Opin Neurol:248-253.
  2. Tso AR, Trujillo A, Guo CC, Goadsby PJ, & Seeley WW (2015) The anterior insula shows heightened interictal intrinsic connectivity in migraine without aura. Neurology:1043-1050.
  3. Liu H, et al. (2015) Resting state brain activity in patients with migraine: a magnetoencephalography study. in The Journal of headache and Pain, pp 16-42.
  4. Tessitore A, et al. (2015) Abnormal Connectivity Within Executive Resting-State Network in Migraine With Aura. Headache 55(6):794-805.
  5. Campbell DA, Tonks EM, & Hay KM (1951) An Investigation of the Salt and Water Balance in Migraine. British Medical Journal:1424-1429.
  6. Bhoi S, Kalita J, & Misra U (2012) Metabolic syndrome and insulin resistance in migraine. The Journal of Headache and Pain 13(4):321-326.
  7. Guldiken B, et al. (2009) Migraine in Metabolic Syndrome. The Neurologist 15(2):55-58.
  8. Sachdev A & Marmura MJ (2012) Metabolic Syndrome and Migraine. Frontiers in Neurology 3:161.
  9. Bigal ME, Liberman JN, & Lipton RB (2006) Obesity and migraine: a population study. Neurology 66.
  10. Tana C, et al. (2013) New insights into the cardiovascular risk of migraine and the role of white matter hyperintensities: is gold all that glitters? The Journal of Headache and Pain 14(1):9.

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Migraines and Hormones: Behind the Curtain

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Angela A Stanton,Ph.D.

Before puberty, migraines are three times more frequent in males than in females but after puberty the tides turn and females are more likely to suffer from migraines than males. An Oxford study found that females are twice as likely to have migraines and that

“brains are deferentially affected by migraine in females compared with males. Furthermore, the results also support the notion that sex differences involve both brain structure as well as functional circuits, in that emotional circuitry compared with sensory processing appears involved to a greater degree in female than male migraineurs.”

The overwhelming belief is that the connection is clear: the hormones kick in for women at puberty and that must be the reason. This begs the questions: 1) Do males have the same hormonal problems before puberty as females do after puberty? If hormones are at root of the problems, then there must be some similarities, right? 2) If female hormones are responsible for migraines, do all females have migraines when they reach puberty? 3) Do migraines cease when hormones stop changing after menopause? 4) What about pregnancy or postpartum, how do hormones impact women then? And finally, 5) Do men stop having migraines after puberty?

Some of the answers to these questions will surprise you and may make you wonder if hormones have anything to do with migraines at all. In this post, I show you that while there are some connections between hormones and migraine they might not be the primary drivers of migraine. The relationship between hormones and migraine is not in the presence of hormonal changes but what those changes require in terms of brain energy, the lack of which causes migraines.

First, I would like to respond in quick the five questions I asked earlier: 1) Do males have the same hormonal problems before puberty as females do after puberty that causes them migraines? The answer to this is no. 2) If female hormones are responsible for migraines, do all females have migraines when they reach puberty? The answer to this also is no. 3) Do migraines stop after menopause? Many women have more migraines and some even start migraines in their menopause, so the answer is no. 4) Do migraine increase or decrease during pregnancy or postpartum? The answer is no during pregnancy, but yes postpartum. 5) Do men stop having migraines after puberty? No they do not.

It is not obvious that the cause of migraines must have anything to do with female monthly cycles and their associated hormones. Given also that many women have migraines after puberty, we are safe to assume that some other factors may play a role. It would be hard to envision a world full of children in which our evolutionary road took women to necessarily experience migraines with their menstrual cycles. So what is the connection to hormones; how do women end up with migraines; and why?

Rather than listing all the hormones that activate throughout the monthly cycle of a woman, let’s take a look at what is happening in the body of that woman backstage, during the hormonal changes. First, in a small review I cover in a few sentences what a migraine is.

Migraine is a collection of symptoms that have an underlying physiological mechanism based on chemical (ionic) imbalance in the brain. Migraine is a neurovascular event that Dr. Charles at UCLA called “spectacular neuro-physiological event” that changes the neurophysiology or chemistry of the brain itself. This can be seen using fMRI technology where oxygenation of brain regions shows where activity occurs during migraine—albeit this does not show why it occurs. The same article also suggests that though medications are available to treat the pain associated with migraines, half the sufferers do not receive any pain relief benefit from the drugs. I find this statement alone interesting because if migraine was truly understood, the pain medication would work for all. This clearly is not the case. To understand what is happening, we must think out of the box and leave behind the hormonal theory of migraines.

Moving Beyond the Hormone Migraine Theory

We now visit the female body all through a month. Let’s start two days after her menstrual cycle has ended. As female, we feel great, no pain, no bleeding, life is awesome. But what we don’t see works hard in the background using up important energy: the brain. Our hormonal changes are happening every moment of the day only we don’t feel it—hormonal changes are directed by the brain. Because we don’t feel the changes, we are ill-prepared for the inevitable day when it reaches a threshold point of not enough brain energy and the migraine starts. This typically happens 2-4 days prior to menses. I do not think migraines are caused by hormones, but rather they are triggered by the lack of energy available to the brain as the hormones cycle. When the brain runs out of energy, a wave of cortical depression begins in some part of the brain. This is what we feel as a migraine.

What actually happens that uses all that energy? After the menstrual cycle is over, the female body immediately prepares for the next menstrual cycle. There is no downtime for rest. The brain turns off one group of hormones and turns on others thereby manipulating how women see the world prior to and during estrus (fertile time). After a menstrual cycle is over, the brain turns on the estrogen to do a few things:

  1.  Prepare the uterus with a new fertile lining to accept the fertilized egg should one arrive and start a new life.
  2. In order to make such fertilized egg happen, the egg must be prepared in the ovaries so hormones initiate the ripening of a new egg.
  3. The woman’s body goes through amazing visible changes at this time of the month. If she had pimples, they magically disappear. If she was bloated, her bloating goes away. Her face becomes the most symmetrical it possibly can; the more symmetrical the more sexually appealing she becomes to the opposite sex.
  4. She becomes extremely attracted to high testosterone males requiring her pheromones to change and to be able to sense a high testosterone pheromone male’s presence. This high testosterone attraction changes after estrus to attraction to low testosterone males for the safety of the child, should mating end in a baby.

With all this activity going on in the female body that she cannot feel, she is in danger of exceeding the threshold of brain energy-shortage without prior notice or preparation. The cost of all of these activities behind the curtains in the female body is very high in terms of brain energy and hydration.  These are sex-hormonal functions that only exist for a certain period of time during the female life. Females are known to be born with all of their eggs they will ever ripen for possible babies. Only these eggs are not “ripe” at birth. Every month one egg ripens in one of two ovaries (sometimes in both and sometimes in none). This egg breaks out of the ovary and starts its journey down the ovarian tube where it either gets fertilized by a sperm or not. If the egg is fertilized, it attaches to the wall of the uterus lining—later to become the placenta of the baby—and a new life cycle begins in the mother-to-be. If however there is no sperm able to penetrate the egg, while it descends in the ovarian tube, the egg will have to be cleared from the uterus together with the nutritious blood vessel rich lining created. This happens with the menstrual bleeding. This we can see and feel.

My Theory: Why Hormone Changes are not the Cause of Migraines

As shown earlier, migraines are not equally present in everyone’s life. Other factors, such as genetic predisposition to sensory organ hyper sensitivities (SOHS) that require more energy, may be the cause. Recent research hints at ionic balance (meaning energy available for use) is crucial in maintaining optimal function and the slightest imbalance can cause major problems (Wei et al.).

When the body is tasked with demanding activities the cells responsible for completing those extra tasks are doing extra chores and need extra energy. The brain regulates the creation of extra hormones for the menstrual cycle. The brain manages the clearing of the uterus after the fertile layer was not used.

By the third day after the cycle, the brain is ordering an egg to ripen—this takes extra energy. This is a once a month event. The brain must have extra energy to complete this task. Ever tried to run a marathon on empty or run your car the extra mile without fuel in your tank? Not possible. Something must break. The brain is the logical one for those who are predisposed to SOHS. If their brain runs out of energy, the neurons cannot generate voltage and stop creating neurotransmitters that instruct the production of hormones in the body. This leads to cortical depression and migraine.

Migraine during Pregnancy

Hands up: how many of you had migraines during pregnancy? Up to 75% of migraineurs do not have migraines during pregnancy. Why you may ask? There is more than one reason for this. The first and most important reason is that while the mom-to-be is pregnant, she has no menstrual cycles so the brain has no monthly cyclical job and it need not use extra energy. Even if the pregnancy comes with a menstrual flow here and there—as it sometimes happens—there is no egg that ripens and there is no uterus layer to remove. It is only a bit of bleeding but no extra energy was needed by the brain for this menstrual flow.

The second important factor is that during pregnancy the mom-to-be seems is more cognizant of what her and her baby-to-be needs. She eat more, tends to eat what she craves and is less likely to be good-looking-body conscious during this time. Pickles with ice cream are famous cravings of women. All the nutrients the brain craves for re-creating energy and feed the brain to prevent migraines: salt, calcium, magnesium, and fat that converts to sugar in the brain.

Migraine during Postpartum

After giving birth nearly, nearly all women immediately revert to eating for a good looking body, lose all the baby fat, and get back into the size zero genes. They stop eating brain-healthy after pregnancy (they never realized they ate brain healthy the first place). Nearly all women return to their migraines postpartum as they return to their old dietary habits.

Post-Menopausal and Menopausal Migraines

We are often told that after we enter menopause or are post-menopausal, our migraines will disappear. Yet, I talk to many women, who have more migraines after their fertile period of life has passed. I am one of those women who experienced more migraines in menopause than in early life. Thus, being no longer fertile, no longer ‘hormonal’ does not mean that we become migraine free; further pointing to the lack of connection of migraines to hormonal fluctuations. In menopause, many women are still very body conscious and watch their dress size more than their health. Others, however, recognize the value of a body supporting diet that may not create a body to fit into such small jeans but may be healthier for an older woman. This second group probably stops experiencing migraines (like I did) whereas the first group remains dehydrated and lacks brain nutrition to work those SOHS brains. They end up continuing their migraines as they had them before.

Of course, we already know from my previous posts that migraines are genetic so not everyone abusing her body will end up as migraineur. To be migraine free, everyone, male or female, must follow the rules of brain fuel.

Fuel for Migraines (Hormonal or Not)

What exactly is the fuel for migraines of any kind? I am leading you back to the first post on migraine that tells you what nutrition the brain needs to return to energy and fuel-filled comfortable homeostasis. The brain works on electricity, which requires specific charge differences inside and outside the cell’s membrane. This voltage is created by salt (sodium and chloride) in ample supply. Sodium also retains water inside the cells for hydrations and opens the sodium-potassium gate to allow nutritional exchange. I am also linking you back to the second post on migraines that explains the anatomy of migraines and what actually happens when the brain in not in homeostasis. How a migraine starts is now visible in fMRI. If you follow the posts I linked to and read the book on how to prevent and fight migraines, chances are, you may never have to face another migraine in your life.

Sources:

  1. Fighting the Migraine Epidemic; A complete Guide. An Insider’s View by Angela A. Stanton, Ph.D. Authorhouse, February 2014. https://www.amazon.com/Fighting-Migraine-Epidemic-Complete-Migraines/dp/154697637X/ref=tmm_pap_swatch_0?_encoding=UTF8&qid=1518636023&sr=8-1 
  2. Why Women Suffer More Migraines Than Men by Patty Neighmond, NOR April 16, 2012 3:17 AM ET http://www.npr.org/blogs/health/2012/04/16/150525391/why-women-suffer-more-migraines-than-men
  3. Her versus his migraine: multiple sex differences in brain function and structure by Maleki et al. BRAIN. 2012: 135; 2546–2559, http://brain.oxfordjournals.org/content/brain/135/8/2546.full.pdf
  4. Hormones & desire Hormones associated with the menstrual cycle appear to drive sexual attraction more than we know. American Psychological Association By Bridget Murray Law. March 2011, Vol 42, No. 3 Print version: page 44 http://www.apa.org/monitor/2011/03/hormones.aspx
  5. Human Oestrus by Steven W Gangestad, Randy Thornhill. The Royal Society, Proceedings B May 2008  http://rspb.royalsocietypublishing.org/content/275/1638/991
  6. Ovulating Women are STRIPPING Men of their Money. Cal Poly Bio 502 class lecture notes article. A blog about human evolution, economics, and sexual physiology. Why do strippers make more money at different times of the month? By Hayley Chilton http://physiologizing.blogspot.com/2013/01/ovulating-women-are-stripping-men-of.html
  7. Migraine and Children. Migraine Research Foundation http://www.migraineresearchfoundation.org/Migraine%20in%20Children.html
  8. Prevalence and Burden of Migraine in the United States: Data From the American Migraine Study II; Richard B. Lipton, MD; Walter F. Stewart, MPH, PhD; Seymour Diamond, MD; Merle L. Diamond, MD; Michael Reed, PhD. Journal Headache; 646:657
  9. Population-based survey in 2,600 women. Karli et al., The Journal of Headache and Pain October 2012, Volume 13, Issue 7, pp 557-565 http://link.springer.com/article/10.1007%2Fs10194-012-0475-0
  10. Multisensory Integration in Migraine Todd J. Schwedt, MD, MSCI. Curr Opin Neurol. Jun 2013; 26(3): 248–253
  11. Unification of Neuronal Spikes, Seizures, and Spreading Depression. Wei et al., The Journal of Neuroscience, August 27, 2014 • 34(35):11733–11743 • 11733

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The Anatomy of a Migraine

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Angela A Stanton,Ph.D.

What is the anatomy of a migraine? Do migraines have an anatomy, a location map, in the same way heart disease does? Sure, migraine happens in the brain and we feel the pain in our head if there is pain – not all migraines come with pain, but does the pain guide us to a causative anatomy of the migraine the same way a heart attack does to the heart? No, it does not; at least not in the same way a blocked artery points to the cause of heart attack. The symptoms of migraines correspond to no specific regions of the brain, except in the case of the aura migraine, which points at the visual cortex. Only about 15% of those with migraines have auras. For 85% of the cases, we do not have the anatomical location of the migraine understood. Most science seems to consider aura and non-aura migraine different in nature and cause. Are they? Maybe not.

Most migraines are not connected to the symptoms we feel (nausea, dizziness, IBS, RLS, anxiety, nausea, vomit, etc.) and because of the variety of symptoms, there is nothing to guide us, such as a scan of the arteries for heart or a stroke. Another contributing factor is that there are no pain sensing nerves in the brain. All pain is felt by the trigeminal neuron receptors that are located on the meninges of the brain. That is, the pain we feel as migraineurs is disconnected from the actual location that causes migraines. To find the anatomy of a migraine, we need to go beyond the symptoms and the pain of the disease, beyond the visible disturbance of the eye in the aura, to the underlying cause for these symptoms.

For much of recent history, migraine research has revolved around two discrete theories of migraines: vascular and non-vascular mental illness. The two schools of thought were merged into what is now called neurovascular disease. But the latest findings suggest that there is more to migraines than neurovascular disease.

Migraine as Vascular Disease

For much of the 20th century, migraine was considered to be a vascular disease. This meant that migraine pain was caused by cranial blood vessel dilation or constriction. Still today we can see many over-the-counter migraine drugs that constrict blood vessels with caffeine in order to constrict the vascular structure of the brain (and the heart and the rest of our body). Alternatively, many doctors still prescribe beta blockers that reduce blood pressure and loosen arteries for easier blood flow and reduced constriction. If migraine is a disease of vascular nature, what causes the cranial vasodilation changes, particularly if these changes do not affect the heart or other parts of the body? This is the first clue that migraines are something more than just vascular in nature.

Migraine as Non-Vascular Mental Illness

The second prominent theory in migraine research attributes migraine pain to alterations in neurotransmitters, specifically, serotonin. Research is confusing on whether migraineurs have less or more serotonin than non-migraineurs. The possible serotonin connection brought us the many prescription drugs containing, increasing, or decreasing serotonin in the brain (triptans, SSRIs and others). Today, most migraineurs receive at least one serotonin enhancing drug; some I know receive serotonin blocking drug but that represents the minority. I was one of the millions of migraine patients who received serotonin enhancers (triptan) and also one of the millions of migraineurs for whom these medications did not work.

Again, I must ask, if there is a serotonin deficiency or overflow in migraineurs, what causes it? And if it is a deficiency as is proposed to be the case for most migraineurs, isn’t this the same proposed deficiency as in depression? Why then don’t most who are depressed also suffer from migraines or why do those who suffer migraines as a result of lack of serotonin not suffer depression? It is not clear to me that there is any connection between serotonin and migraine since most migraineurs I know are not at all depressed and most depressed do not have migraines. This tells me that something is not right with the concept of identical treatments for such two completely different illnesses.

Serotonin is created by a normally functioning brain. Why it is deficient, or in some cases, elevated in the brain of migraineurs has always puzzled me. It still puzzles me that others didn’t ask why neurons cannot produce the right amount of serotonin on their own or why physicians so easily prescribed drugs to add or enhance what the brain was not making. Should we not find out why the neurons are not producing serotonin in the first place? Wouldn’t this help us better treat and maybe even cure migraines?

Migraine and New Research

The most recent theory about migraines involves the aberrant electrical discharges associated with migraine and a phenomenon called cortical spreading depression:

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. (Lauritzen et al., J Cereb Blood Flow Metab)

Researchers have linked CSD to the eminent onset of migraine pain. Such a rapid change in brain ion homeostasis can affect changes in neurotransmitter concentrations, causing cranial vascular dilation and ionic imbalance with depolarized regions. These changes can evoke what migraineurs sense as pain but one has to ask by what mechanisms are these ionic brain changes initiated and by what pathways do they elicit the pain. For the first question, let us return to the concept of neural dehydration and salt deficiencies as possible instigators.

A Unified Theory of Migraine Pain

A new report shows migraines, seizures and strokes are all about ion (sodium, potassium, chloride, magnesium, and oxygen) homeostasis. These particular models looked at how changing potassium ion concentration affects brain activity and how seizures and migraines have similar underlying mechanisms. Potassium’s job is to work both inside and outside of the neurons helping to balance homeostasis by ensuring that potassium ions are in the correct place all the time. Potassium is a diuretic substance and helps in the removal of excess or used water from the cell. If there are too many potassium ions inside or outside of a neuron, with all else remaining constant, the neuron will end up dehydrated because of the osmotic gradient.

The overabundance of potassium and a depletion of both extra-cellular sodium chloride reduces water, and changes the pH balance (acidic level) of the neuron (Costa et al., The Journal of Headache and Pain). Recall from my earlier post: Dehydration and Salt Deficiency Trigger Migraines, that channels on the membrane of the neuron allow for leaks using osmotic gradient to balance the internal and external ionic content. Because ionic homeostasis balance is required for a healthy brain, the ionic balance must be true for all electrolyte elements, including sodium as well. Not enough sodium can cause a potassium overabundance that can trigger migraines because the neuron is not able to generate electricity or retain water.

In  Dehydration and Salt Deficiency Trigger Migraines, I talked about the importance of hydration and explained how that works at the cellular level. I introduced the sodium-potassium pumps and their role in keeping the cell hydrated. Through the sodium-potassium pumps sodium ions and potassium ions head in and out of the neuron when proper electric currents are established. For the electric current, the ionic balance of sodium and chloride is essential so that the pumps can open and close. There are also osmotic channels through which leakage of ions may happen depending on higher or lower levels of ions inside versus outside the cell—the osmotic gradient.

The phenomenon of cortical spreading depression is a slow spreading electrical surge corresponding to depolarized regions of migraine initiating locations. It is initiated by ion imbalance where the normal homeostasis has been lost. Here the sodium-potassium pumps do not function properly; the channels leak too much potassium and water, magnesium and oxygen out from the neuron. If these ions cause imbalance, trouble ensues. Even a small, unnecessary increase in potassium outside the cell can lead to seizures and by association to migraines.

It’s All About the Ions

So, beneath the vascular and non-vascular definitions of migraine, the neurotransmitter imbalances and the hyper-excitability of neurons in the certain brain regions associated with migraine, are simple variations in ionic balance, responsible for the onset of migraine and the possibility of vasoconstriction or relaxation changes as a consequence. Too much or too little of one or more ions, evokes changes in brain’s electrical activity that can lead to migraines or seizures. Where in the brain those changes occur determines the type of symptoms a migraineur experiences. For example, with aura migraine the anatomical initiating migraine location is the visual cortex. The migraineur sees the aura with eyes also closed. So what the migraineurs sees is happening inside the brain and not outside. The visual cortex’s function is to translate the light signals it receives into meaningful images of objects. The CSD is an electric storm that the visual cortex interprets as aura. The aura usually starts with a blind spot. It is my belief that the blind spot represents the region of neurons that is the cause of the migraine; the depolarized region that the CSD is trying to activate.

Concluding Remarks

The overall neuron-behavior is very complex but today we can say with a high degree of conviction that:

  • Migraines are caused by malfunctioning neurons as a result of ion imbalances.
  • Ion imbalance can be visualized by regions of depolarization.
  • Depolarized regions demonstrate the anatomy of the disturbance.
  • Hydration and maintaining proper ionic balance (correcting salt deficiency, magnesium deficiency, potassium excess or deficiency) is important for migraineurs since the slightest ionic imbalance can cause a migraine.

From my perspective, I am glad to see the most recent attempts at understanding physiological problems in the brain behind the migraine. This is a very important shift in migraine research – looking beyond the symptoms for a cause. Nevertheless, I am still looking for answers. How does the ion balance become so disturbed that it initiates a migraine? Why does this happen for some folks and not others?  Those are the questions, researchers and clinicians need to address. My theory is that the depolarized regions of the brain result from disturbances in homeostasis and ion balance which are precipitated by dietary deficiencies. We need to determine the proper amounts of each mineral and micronutrient required for the well-functioning brain to reduce migraine.

Sources:

  1. Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury. Martin Lauritzen, Jens Peter Dreier, Martin Fabricius, Jed A Hartings, Rudolf Graf, and Anthony John Strong; J Cereb Blood Flow Metab. Jan 2011; 31(1): 17–35. Published online Nov 3, 2010. doi:  10.1038/jcbfm.2010.191 PMCID: PMC3049472
  2. Cortical spreading depression as a target for anti-migraine agents. Cinzia Costa, Alessandro Tozzi, Innocenzo Rainero, Letizia Maria Cupini, Paolo Calabresi, Cenk Ayata and Paola Sarchielli1; Costa et al. The Journal of Headache and Pain 2013, 14:62
  3. Interpreting fMRI data: maps, modules and dimensions. Hans P. Op de Beeck, Johannes Haushofer & Nancy G. Kanwisher Nature Reviews Neuroscience 9, 123-135 (February 2008)
  4. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Hadjikhani N1, Sanchez Del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK, Cutrer FM, Rosen BR, Tootell RB, Sorensen AG, Moskowitz MA. Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4687-92. Epub 2001 Apr 3.
  5. Unification of Neuronal Spikes, Seizures, and Spreading Depression. Yina Wei, Ghanim Ullah, and Steven J. Schiff ; The Journal of Neuroscience, 27 August 2014, 34(35): 11733-11743; doi: 10.1523/JNEUROSCI.0516-14.2014

 

 

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