The anxiety I now associate with visual alterations is indescribable.  Maybe I am the only person that experiences little white floaters in my line of vision, but I thought everyone did.  Seriously, for a long time I thought everyone had these and they just came and went sporadically.  Don't worry I have had my eyes checked fairly regularly over the years.  So, I am quite certain I don't have any retinal detachment going on.  No, not retinal detachment or any other actual eye disease, just strange brain activity (and I am not certain that is better).

These visual disturbances start with a little white spot on just one side of my visual field.  It's either on my right or left eye...but never both at once.  It's there when my eyes are open and it's there when my eyes are closed.  I can't run and hide from it or blink it away.  As the time ticks by, the little white spot starts to elongate.  It gradually becomes  curved flickering white line in the upper lateral quadrant of my visual field.  Eventually the flickering line pushes up and out of my visual field entirely.  The entire process lasts about 30 minutes for me.

This particular visual disturbance is very elusive to me.  It doesn't always precede a pounding headache.  Sometimes it comes alone and it disappears without any pain.   Sometimes it appears when my alarm goes off in the morning, which makes me wonder if it is healthy to have a startling noise wake me from my deeply needed slumber. 

What I experience is a "classic" presentation of an ocular migraine or aura.  The flickering lighted line is known as a "scintillating scotoma".  If you are like me you have wondered how this visual alteration occurs.  What makes me see spots?  The experts believe that this is a neurovascular event.  It involves the firing of nerve cells in the brain and nerve cell activity affecting the blood flow in the brain.  There is an overstimulation of cell firing and then a depression of activity in the brain.  You may hear the term "cortical spreading depression" used to describe this cell firing behavior change.  The process begins with blood vessels spasming and constricting blood flow.  This constriction affects the conductivity between nerve cells causing a disruption along the visual cortex (part of the brain responsible for seeing).  As the disrupted firing crosses the visual cortex it causes us migrainuers to see the flickering lighted line.  It takes around 20 minutes to completely cross the visual cortex wich corresponds with the length of time spots are seen.  If your symptoms end with the scintillating scotoma, it probably means the electrical cell disturbance stopped at the end of your visual cortex.  If you are unfortunate enough to experience other symptoms: facial or extremity numbness and tingling or nausea and vomiting it means the electrical disturbance wasn't finished when it got to the end of your visual cortex and decided to go ahead and mess with other areas of your brain as well.

**The picture shown is an artist's rendition of a scintillating scotoma found on Wikipedia.  You can see more examples of what a scintillating scotoma looks like by clicking here.






 

**Pictured: BPA free drinking cup along with disposable plastic water bottle.

Fairly recent research suggested a connection between drinking out of plastic bottles and increased association with migraine: Exposure to Bisphenol A Exacerbates Migraine-like Behaviors in a Multibehavior Model of Rat Migraine.  The study results showed an increase in what the researchers identified as migraine-like behaviors in rats (decreased locomotion, light and sound aversion, altered grooming habits, and enhanced startle reflexes).  Results also showed alterations in estrogen signaling and changes in nociception (basically pain receptor processing).

BPA is a chemical in plastics.  It is in plastic bottles, dental sealants, medical devices, lining of canned goods, etc.  Most of us, 90% have BPA present in our bodies.   This is primarily due to consumption of food that has been in containers made with BPA.  It is considered an environmental estrogen because it acts like estrogen in the body.  In the body it can cause estrogen levels to rise and change the internal hormonal balance which may trigger a migraine as well as cause other problems.

I do know that fluctuations in estrogen levels is a trigger for most people with migraines.  I don't think plastic is the main reason for my migraines, however, I consider it a potential trigger.  Back when I started my migraine plan, I started eating mostly real foods, no packaged foods, very rarely a canned item (green chilies is the only item I can think of that I consume from a can).  So, it may be possible that I inadvertently eliminated most of my BPA exposure when I changed my diet.  When I am at home I usually drink from a glass or mug, not plastic cups and I am not a huge consumer of plastic bottles.  That being said when I am in an airport I always buy a plastic water bottle (maybe I should start supplying my own drinking container when traveling).

I guess migraines aren't the only problem associated with BPA. The FDA used to say BPA was safe, but changed their statement in 2010 stating that studies show "current levels" of human exposure are safe.  They have also expressed concern over the potential effects on the brain, behavior, prostate glands in fetuses, and young children. Here is a list of potential problems according to WebMD:

1. Hormone Disruption
2. Brain and behavior effects
3. Cancer
4. Heart problems
5. Possible connection to "obesity, diabetes, ADHD, and others."
6. Possible risk to developing bodies of infants and young children.

When I started my Migraine Plan a year and a half ago, I eliminated a lot of BPA simply as a result of preparing all of my own food.  I started eating a lot more whole and organic produce and meats and a lot less packaged and canned foods.  It looks like data shows more than one reason to reduce BPA exposure.  Here's my plan to do that:

1. I will make sure plastics I am using are BPA free. Get rid of plastics with the number 3 and 7 on the bottom, which are more likely to contain BPA.
2. I will use non-plastic or BPA free food containers and bottles for drinking and food storage.
3. I will not ever heat plastic items...this causes BPA to leach out.
4. I will get rid of plastic items that are old and cracked or scratched.
5. I will not to use canned items or choose brands that use BPA free cans.

I came across a scary social media advertisement lately that looked like this...

Scary because as a mother of small children...we do eat hot dogs in our house.  That being said as a result of my migraine influenced diet, I purchase organic hotdogs without nitrates or nitrites.  Nitrates and nitrites are a published migraine trigger.  But the statement made in the picture definitely made me think about and research the facts surrounding hotdogs and childhood leukemia.  This picture above was based on the following research conducted at University of California Medical School: Processed Meats and the Risk of Childhood Leukemia.  There has been other research that has conflicting results: Food Consumption by Children and the Risk of Childhood Acute Leukemia.  The one thing the health community does agree on is that processed meats, including bacon, deli meats, and hot dogs are linked to increased colorectal cancer.  They aren't sure what exactly the main culprit is, but experts recommend steering clear of the preservatives sodium nitrite and sodium nitrate.

As Americans we live in a culture where packaged foods is more common than not.  The food industry is always looking for ways to increase shelf life and reduce cost.  The additives that accomplish these goals affect some of us differently than others.  Sodium nitrate and nitrite are added to meats to preserve the color and decrease bacterial growth.  Sodium nitrite is used in the curing process to slow the development of botulism, add flavor, keep the meat pink, and increase shelf life.  Sodium nitrate is converted to sodium nitrite in our bodies and fights botulism.  Both nitrate and nitrite create nitrosamines when combined with protein rich foods which leads to cell damage in our bodies.

What does all this have to do with migraines?   I realize cancer and migraines are too very different things but apparently the culprit in both cases are believed to have something to do with nitrates and nitrites--not necessarily hot dogs.  When we consume these preservatives nitrite becomes nitric oxide.  Nitric oxide binds hemoglobin (iron-containing oxygen-carrying protein in our blood).  Once bound to our hemoglobin it decreases the amount of oxygen that hemoglobin can carry.  Nitric oxide is also a vasodilator.  It causes blood vessels to enlarge and dilate.  When this dilation occurs in the blood vessels in our heads it can trigger a migraine.  There is also a theory that the nitric oxide stimulates the release of calcitonin, a hormone that affects the nerves in brain vessels.

A recent study may have found a biomarker for migraines!  What does this mean to the migrainuer?  Well, let's just start with the physiology behind this biomarker (CGRP)...

During a migraine, trigeminal (the largest cranial nerve) activation leads to a release of a nueropeptide called CGRP.  The release of this nueropeptide leads to peripheral inflammatory and vasodilatory responses that trigger nuerons involved in pain transmission. These events cause the stereotypical throbbing pain experienced during a migraine.  I don't know if you read my post about estrogen and migraine.  In it I mention the nueropeptide, CGRP which is released with a drop in serotonin causing vasodilation.  A new study showed levels of CGRP are elevated in the peripheral blood of women with chronic migraine.  These elevated levels were found in the absence of both migraine attacks and medication.

For this study they were able to round up 103 chronic migraine sufferers (women with 15 or more headache days a month for at least 3 months).  The control groups were 43 matched women with episodic migraine,  and 31 matched healthy women without a headache history, along with a series of patients with 14 episodic cluster headache matched for age in a pain-free period.  They drew blood on migraine-free days where no symptomatic medication was taken the day before the blood draw.  Patients were allowed to take daily preventive medication.

The study authors concluded that elevated levels of CGRP in the absence of a migraine could be a biomarker for patients with Chronic Migraine.

So what does that mean to the chronic migrainuer?  Maybe your illness will no longer be invisible.  There will be scientific proof that your throbbing pain does exist and it is real.  CGRP levels could be drawn to confirm the diagnosis of chronic migraine.  It also makes me wonder if treatment research will be aimed at decreasing CGRP as therapy for the migrainuer.

If you are a woman experiencing migraines it is almost certain that like me, you have noticed some sort of correlation between your cycle and your migraines.   Although chronic migraine may make it difficult to identify estrogen cycle fluctuations as your trigger due to migraine frequency.  So what about our cycles makes us susceptible to migraines at specific times versus others?  There have been numerous studies suggesting a connection to estrogen.

If we take a look specifically at estrogen during a female cycle, this is what happens:
1. Menstruation: estrogen typically measures at a low of <50 pg/ml (first 7 days of graph)
2. Follicular development: estrogen increases during follicular development and peaks at about 200 pg/ml (peak pictured in graph)
3. Ovulation: estrogen drops briefly during ovulation (around day 16 pictured in graph)
4. Luteal phase: estrogen rises again for a second peak (roughly days 20-24 pictured in graph)
5. End of Luteal phase: estrogen level drop to their menstrual levels (assuming we aren't pregnant)

For me personally I tend to "struggle" around (1.) menstruation and (3.) ovulation.  These are both times in the female cycle where estrogen is dropping.  Estrogen related migraines usually are due to a drop in circulating estrogen after exposure to higher levels of estrogen for a few days (this is referred to as estrogen priming).  This "priming" happens naturally at the beginning of menstruation or immediately after giving birth (and lucky me, after delivering both of my beautiful children I had a tremendous migraine).

Other instances that can cause a change in estrogen levels include:
1.  A purposeful withdrawal from an estrogen containing product (birth control) during the hormone-free week or interruptions in estrogen therapy.
2. Unintentional withdrawal from estrogen by missing doses of pills or as a result of drug interactions that may reduce estrogen availability.

This made me wonder exactly how and why does this drop in estrogen trigger a migraine? 
While investigating I came across a connection between estrogen and serotonin.  Estrogen may also impact migraines by affecting other chemical mediators like nitric oxide, magnesium, and prostaglandins which help keep balance between
excitatory and inhibitory neurotransmission.  However I find the estrogen-serotonin connection particularly interesting.  If you are familiar with migraine medications then you know that one of the most effective abortive medications for migraine are a class of drugs called triptans.  These drugs are serotonin receptor agonists (meaning they bind to the specific receptors in the brain that bind to serotonin).  They work because once they bind that receptor on cranial vessels they cause vasoconstriction (shrinking of the vessels) as well as a decrease the release of a neuropeptide that causes inflammation.  Estrogen impacts the central nervous systems in a number of ways.  When estrogen levels drop, serotonin levels fall and there is also an increase in the rate of serotonin elimination.  With the drop in serotonin two things happen that could impact a migraine: a release of calcitonin gene-related peptide (which is a potent vasodilator or vessel expander that is produced in both peripheral and central neurons) and a release of substance P (which is associated with pain and inflammation) from trigeminal nerves.  To sum it all up, this drop in estrogen has begun a process that leads to vasodilation of cranial blood vessels and pain and inflammation via the trigeminal nerve.

**My graph of the female hormones during cycle was made available thanks to Wikipedia
 

Migraine is not a headache.  I know that sounds weird, so let me explain.  Saying a migraine is a headache would be like saying Chixenpox is an "itch", or saying getting hit in the shin is a "bruise", or saying bronchitis is a "cough", or saying the stomach flu is a "vomit".  I may be getting a little carried away with my analogies, but hopefully I made my point.

Headache is a symptom associated with migraines.  It is how most of us with migraine suffer.  The classic migraine presents with one-sided head pain that is pulsating in nature accompanied by nausea, sensitivity to light and sound.  However, not all migrainuers present the same way.  Unfortunately, headaches aren't our only problem.  Some people present with cyclical vomiting.  Some people go blind.  Some people have abdominal migraines with intense abdominal pain and nausea.  Some people have stroke-like symptoms.  We are all made just a little differently, and so we all present a little differently, which makes us a difficult group to diagnose, treat, and understand.

You are probably wondering if it isn't a headache what is it? It is a neurologic/neurovascular disorder.  One thought is that there is an increased excitability of the cerebral cortex that coincides with abnormal control of pain neurons in a specific part of the brainstem.  They believe the malfunction begins in the brain and spreads to blood vessels.   There is some uncertainty as to whether the neuronal mechanisms or blood vessels play a greater role.  There is also some evidence that altered levels of nuerotransmitters may be involved in the migraine process. 

To complicate migraines and their treatment more, migraine also comes with a slew of comorbidities (the presence of other conditions) that include cardiocerebral, vascular, psychiatric, metabolic, and neurologic pathologies.  Much more research is needed in this field so that we migrainuers can be adequately be cared for.  June is migraine awareness month and  this migrainuer has spent many a day trying to figure out my own body enough to be able to manage my own migraines.  I know that every individual is different with different comorbidities and management strategies.  After successfully managing mine for a little over a year I created my site in an attempt to help others that may benefit from my strategy and migraine plan or anything else I can provide to a fellow sufferer.  I am not naïve enough to believe that my plan will help everyone, but only hope it will help someone...although it would be wonderful if it could help everyone:)!

If you feel inclined to support further research and support for migraines here are some great migraine organizations:

1.  Donations to the Migraine Research Foundation can be made to help the continued search for a better understanding and treatment for migraines.

2.  Donations can also be made to the American Headache and Migraine Association which is an organization which attempts to help empower patients, families and friends through education, support, advocacy, and research.

Let's do whatever we can to end the suffering as a result of this illness!

Whew!  Safe here in Tulsa after a tornado originated very close to my home and touched down near friends last night in Broken Arrow.  This weather is scary and exhausting.

Last week was a rough one for those of us living in Oklahoma.   Depending on where in Oklahoma you were life was a little more fragile but emotions and grief  were high no matter where you were.  We all know the risk that comes with living in this part of the country.  However, we also become a little numb to the warnings after years of getting in our closets.   The tornado drills at schools start at a very young age.  We are trained early to file ourselves into the hallways away from the windows, to get as close to the center of the structure as possible and then to curl up into a little ball and place our hands over our heads and then wait.  We are instructed to locate the safest room in the house.  In my case that room has typically been a closet.  Even though we follow the safety protocols that have been drilled into us since elementary school most of us do so expecting to come out of the closet at the end of the storm to learn the tornado passed through without insult or injury to anyone.  The Moore Tornado last week put all of this training into perspective as well as stripped away the numbness that had built up over the years and left most of us raw and exposed to the emotions that lay in the wake of the devastation. 

So, whether it was tears of sadness and pain from losing precious lives or whether it was tears of amazement in awe of the generosity and miraculous resolve of the human spirit, tears were shed.  As if the barometric pressure changes weren't enough for the migrainuers living in Oklahoma the past few weeks the outburst of tears and strong emotions were a  problem as well.  The knowledge that a good hard cry will most likely precipitate a migraine attack prevents me from allowing myself a good hard cry.  When I feel the tears begin to swell I quickly distract my brain and gather my emotions to become this stoic little robot the migraines have created.  My heart is extremely heavy on the inside but in no way shape or form can I allow myself to relax and let the tears turn into an uncontrolled cry.

Why would crying cause a migraine? 
I believe, along with several scientist that it is worth looking further into for some answers.  There is not much in the literature on crying being a precipitating factor for migraines.  In an attempt to examine the role of crying as a trigger these scientists enrolled 163 migrainuers in their study.  Crying was identified as a trigger by 55% of participants.   In this study the only other triggers listed greater than crying were stress, anxiety, and menstrual periods.  These scientists concluded that since the physiology of crying is not well documented or understood, but it seems to be a migraine trigger, crying warrants further research.

Here are some of my hypotheses with regards to why crying may trigger migraines:
1.  Intense emotions start the process.  This stressful state may be enough on its own to be a trigger. 
2.  Physiologically there is an increase in pulse and respirations, muscles in the head, face, and neck become tense.  This tension may irritate the trigeminal nerve which is linked to migraines. 
3.  The tears themselves may contribute to water loss and hence have a dehydrating effect.  
4.  Crying causes facial and sinus congestion which is a trigger for many a migrainuer.

Typically, I like to present solutions on this blog.  I am not sure we can always stave off a good cry and maybe you could try hydrating if you can't hold back the tears.  So, my solution to my tears and tornados is contributing to the rebuilding of the areas devastated by last weeks storms.   If you haven't already contributed here are some links that might be helpful:
1.  Lifechurch.tv has ways to help either through donations or volunteer on their site
2.  Donate to the United Way Oklahoma Tornado Relief
3.  Volunteer Opportunities on OKStrong
4.  Donate to OKStrong
5.  Also, participating Starbucks will be taking donations this week for OKStrong in exchange for a free cup of coffee!

Prayers to all those that have suffered as a result of this storm.  If you can handle some tears my friend Lisa lost her brother last week in Moore and the rescue worker who found his body was her angel through this tragedy.  Here is a link to their story: http://newsok.com/article/3833849.
 

Have you ever heard of an abdominal migraine?

When I was in my 20s and early 30s I suffered from severe abdominal pain and cramping that would last for hours at a time.  During these painful intestinal aches it was all I could do to go about my normal business.  Along with the stomach pain I felt washed out, pale, tired and sickly.  All I wanted to do during the pain was to seek a dark quiet bedroom and rest in the fetal position. When I sought care for this paroxysmal pain in my 20's I was diagnosed with irritable bowel and put on a prescription drug called Midrin.  Needless, to say the Midrin didn't stop the attacks and eventually over time and with a change in work environment (switching from night shift to day shift in nursing) the painful episodes stopped.  They returned in my early 30's. After dealing with them for a lengthy period of time I sought out a gastroenterologist. I was scoped and tested and worked up for everything from  lactose intolerance to crohn's disease.  Eventually the GI specialist gave up and told me they couldn't find anything wrong with me.  In my mid to late 30's these abdominal migraines converted into a "typical migraine".  For me the typical migraine is unilateral severe head-throbbing pain with sensitivity to light and sound accompanied by eventual vomiting.  When I started having 12 day long migraines where I couldn't stand without vomiting, I picked up a book called the "The Migraine Brain" by Carolyn Bernstien in an attempt to better understand my illness.  In that book is a chapter entitled "Kinds of Migraines".  That was the first time I had ever heard of an abdominal migraine and I immediately had an "ah-ha moment". 

Abdominal migraines are often misdiagnosed (as you can see by my experience).  Diagnostically, the Abdomial Migraine usually occurs in children and isn't diagnosed until a "typical migraine" appears in their history.  The requirements for diagnosis are at least five attacks of abdominal pain lasting 1 to 72 hours unsuccessfully treated.  The abdominal pain is midline, around the belly button (that is my technical term) or poorly localized.  The pain can be dull with a moderate to severe intensity.  The pain is accompanied by things like anorexia (who wants to eat when your belly hurts all the time?), nausea, vomiting, pallor.  The pain can't be attributed to any other disorder.  The abdominal migraine is a sudden episode of intense, acute periumbilical pain that lasts more than one hour.  It has intervening periods of health.  The pain interferes with normal activities and is associated with anorexia, nausea, vomiting, headache, photophobia, and pallor.  There is no evidence of an inflammatory, anatomic, metabolic, or neoplastic (cancerous) processes that explain the subject's symptoms.  The diagnosis is established by history, which includes the above symptoms with wellness between episodes and no alternative causes, and a family history of migraine among relatives.

I am hopeful that using my Migraine Plan will also relieve the pain of those experiencing abdominal migraines.

This blog is dedicated to Lynet and her son.  This migrainuer is so hopeful for you both!