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Identify Your Triggers, Break Dependence on Medication, Take Back Your Life
By Sharron E. Murray
Red Wheel/Weiser, LLCCopyright © 2013 Sharron Murray, MS, RN
All rights reserved.
Understanding Migraine Disease
In the last few decades, research about migraine headaches has come a long way. For example, a migraine headache is now believed to be a symptom of a more complex disorder, migraine disease. A number of theories have been proposed to explain the cause of our disease. Let's take a look at some of them.
The Vascular Theory
For much of my life, medical researchers believed migraine was a headache related to changes in the blood vessels in and around our brains. When exposed to triggers, which I explained in the Introduction as events capable of provoking our migraine attacks, our arteries narrowed. This constriction reduced blood flow and oxygen delivery to our tissues. As our constricted arteries expanded and tried to gain more oxygen, fluid leaked into the surrounding tissue and chemicals such as prostaglandin, which enhances the sensitivity of pain endings and stimulates the release of inflammatory agents, were released. This was known as the vascular theory.
Recent theories suggest that migraine is a neurological disease, which involves more than dilation and constriction of blood vessels. Evidence suggests we have an inherited disruption in brain function that makes our brain cells more excitable than others. When exposed to triggers capable of provoking a migraine attack, a chemical imbalance occurs in our brains. Levels of neurotransmitters (chemical messengers that pass information from one cell to another), such as glutamate, serotonin, dopamine, and norepinephrine, are altered. The most recent theories implicate one or more of these neurotransmitters as culprits in our disease. So, what are these recent theories?
Cortical Spreading Depression Theory
The cortical spreading depression theory believes that a wave of hyperexcitability spreads across the outer layer of our brain (the cortex), followed by a period of suppression. When brain activity is depressed, inflammatory mediators are released. These inflammatory mediators irritate the cranial nerve roots, in particular the trigeminal nerve, which conveys sensory information for much of our head and face.
Glutamate, a neurotransmitter present in the trigeminal nerve, is thought to play a role in the cortical spreading depression. As well, a neurotransmitter found in the brain and spinal cord and known as substance P is thought to coexist with glutamate. Substance P is believed to be involved with the inflammatory process, vasodilation, smooth muscle contraction, nausea and vomiting, regulation of mood disorders such as anxiety, and the sensation of pain.
The Serotonin Theory
Serotonin, also known as hydroxytryptamine or 5-HT, is believed to have a major role in migraine disease. The serotonin theory suggests that we have a defect in a specific type of serotonin receptor that causes our blood vessels to constrict, or narrow. As a result, in the presence of certain triggers, arteries that supply blood to our brain dilate, or expand. The dilation, or stretching, of the arteries in and around our brain causes fluid to leak into surrounding tissue. The fluid leak damages tissue cells and stimulates the release of inflammatory agents, which contribute to the swelling of the arteries and surrounding tissue, leads to irritation of nerves, and intensifies our throbbing pain. Also, because serotonin enhances endorphins (a natural analgesic found in the gray matter of the brain) and has an effect on substance P, low levels of serotonin further exacerbate our pain.
Besides alterations in cerebral blood flow and the sensation of pain, changes in the levels of serotonin are thought to be responsible for a number of gastrointestinal symptoms such as nausea, vomiting, and diarrhea that many of us experience during an attack. This is because serotonin is also a neurotransmitter for the enteric nervous system, or ENS, which is located in the abdomen (ninety-five percent of the body's serotonin is located in the gut). Often referred to as the second brain or gut brain, the ENS causes contraction of the smooth muscle of the gut that is important for normal digestion and the movement of food through the intestines (peristalsis). As well, it regulates intestinal blood flow, the transport of mucosal water and electrolytes, and propulsive bowel function.
Blood levels of dopamine and norepinephrine are believed to fluctuate with our serotonin levels. All three of these neurotransmitters may be responsible for many of the other symptoms we exhibit as our migraine attack progresses. For instance, high levels of serotonin may make us feel calm, full, relaxed, and even drowsy. Low levels may cause us to feel anxious, irritable, and depressed. They may also promote food cravings for starches and sugars, like crackers, chips, ice cream, and chocolate.
An increase in dopamine and norepinephrine levels may make us feel more energetic, focused, and alert. A decrease in these levels may contribute to the fatigue, inability to concentrate, yawning, nausea, and vomiting many of us experience.
The Integrated, or Unifying, Theory
The integrated or unifying theory suggests that both vascular and neural influences cause the pain associated with migraine headaches. This theory suggests that stress and other triggers cause changes in the levels of epinephrine in our bodies, which affects serotonin levels. Fluctuations in serotonin levels cause blood vessels to constrict and dilate. Chemicals, such as substance P, are released and further irritate nerves and blood vessels and enhance our pain and inflammation.
Defining Migraine Disease
The organization MAGNUM (Migraine Awareness Group: A National Understanding for Migraineurs) refers to migraine as an organic neurological disease. Although the importance of the role of one theory over another is debatable in the literature, the disease itself seems to be related to a complex series of events that results in a breakdown of communication between the neurotransmitters in our brain and, as more recent research suggests, in our gut. When exposed to controllable or uncontrollable triggers, which you read about in Chapter Three, a chain reaction is initiated that sets off a cascade of events referred to as a migraine attack.
What Is a Migraine Attack?
A migraine attack is the episodic event we endure in the presence of an appropriate trigger. The attack has been split into four phases: the prodrome, aura, headache, and postdrome. Not all of us go through each phase. For instance, you may never have a prodrome or an aura. Other migraineurs may have a migraine attack without a headache. A migraine attack may last for several hours. Let's take a look at these phases.
Anywhere from forty to sixty percent of us have warning signs that may present a few hours or up to two days prior to the onset of a headache. Our symptoms reflect fluctuations in the blood levels of the neurotransmitters and endorphins I just discussed.
In my case, a couple of days before the headache would break, I would have a period of hyperactivity and feel on top of the world. Then I would become irritable and so fatigued that it was difficult to hold my head up. I would have an increased sensitivity to light and sound, which made it difficult for me to watch TV or go to a movie. My neck became stiff and painful, and I craved salty foods like soda crackers. My face, eyelids, and abdomen would swell and remained swollen until the migraine subsided. My husband would take one look at me and say, "You are going to have a migraine." He became so familiar with the sight, he was able to tell his secretary, who also suffered from migraines, she was going to have an attack and send her home.
You may relate to some of these symptoms or have others including
Change of appetite (anorexia)
Difficulty in concentration
Depression (become withdrawn)
Diarrhea or constipation
Euphoria (feeling high)
Food cravings (sweet, fat, and salty)
Slurred or rapid speech
Approximately twenty percent of us have an aura that develops over five to sixty minutes prior to a headache. The symptoms, thought to be related to the cortical spreading depression theory I previously discussed, may occur in isolation or precede or accompany the headache phase. They should disappear with the end of our aura, or migraine, and may include
Changes in the way we see: For instance, flashing, zigzagged, or brightly colored lights that progress outward from the center of our visual field. Or a blind spot or hole in our visual field. On occasion, I've experienced a hole in my visual field accompanied by brightly colored, zigzagged lights and found the experience to be most alarming. More often, for me, blurred vision was a sure sign a migraine was on my horizon.
Changes in sensation: For example, pins and needles on the hand and arm on one side of our body, or around our nose and mouth on the same side of the body. Or we may have prickly or burning sensations, or muscle weakness, on one side of our body. A word of caution: It's important to note that motor deficits and paralysis are rare and an indication for you to seek immediate medical attention.
Changes in hearing: For instance, we may hear music playing or a clock ticking.
Changes in smell or taste: For me, another sure sign of an impending migraine is the smell of cigarette smoke, even though no one around me has a lighted cigarette.
Changes in the way we speak: For example, we may speak incorrectly, or be unable to recall the words we want to say. In my case, I would speak so fast that I would trip over the words I wanted to say. Many times, in particular when I was giving a lecture, my audience was forced to ask me to slow down.
The intense, throbbing pain typically associated with migraine headaches may be on one side of our head (unilateral), both sides of our head (bilateral), or behind our eyes. Our pain may be aggravated by light, noise, and odors. An increase in physical activity may exacerbate the pain or, in some cases, may relieve our agony. The accompanying symptoms, again, may be related to fluctuations in the blood levels of neurotransmitters and endorphins. The headache may last from four to seventy-two hours, or sometimes longer.
In my case, the associated symptoms like nausea and vomiting were as debilitating as my headache. I was trapped. Tied to my bed afraid to move, not a single digit, finger or toe, lest I had to dash to the bathroom and hang over the toilet bowl until the retching that threatened to blow my head apart stopped. In between the bouts of vomiting, I'd lie beneath a heavy load of blankets and shiver with cold. To make it worse, I had a continuous nasal drip and nasal congestion so severe that I had to breathe with my mouth hanging open, and if I should be lucky enough to fall asleep, wake up with my tongue glued to the top of my mouth and gasping for water.
Again, sound familiar? You may relate to the nausea and vomiting, shivering, runny nose (rhinorrhea), and dehydration, or have other symptoms, which may include
Inability to concentrate
Irrational emotions such as fear, depression, nervousness, anxiety, and panic
Loss of appetite
Sensitivity to touch (allodynia), sound (phonophobia), and light (photophobia)
Tearing of one or both eyes (lacrimation)
After all that, the migraine is not over. For some of us, it may take hours, others days, before a hangover effect disappears. The symptoms we experience are often attributed to the medications we've ingested to stop the pain and vomiting but, again, may be related to those pesky neurotransmitters and inflammatory agents. As I did, you may feel drained of energy, have a lowgrade headache and sometimes a reoccurrence of the headache. Fatigue, irritability, and tender and sore muscles of the head, face, and neck may also be bothersome.
A Word About the Nervous System
The nervous system is composed of the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS is made up of the nerves in the brain and spinal cord. The PNS is divided into the autonomic and voluntary nervous systems. The voluntary nervous system allows us to control movement of the muscular and skeletal systems. The autonomic nervous system is divided into the sympathetic and parasympathetic systems.
The sympathetic system is our "fight or flight" primitive response to pain, danger, or stress. The parasympathetic system is our slow down, or relaxation, response that lowers heart rate and blood pressure and regulates digestion. The enteric nervous system (ENS), which I discussed earlier, is believed to be associated with, although somewhat independent from, the parasympathetic nervous system.
It's important for you to understand that often our migraine attacks can activate our sympathetic nervous system. Besides increasing levels of norepinephrine in the blood, levels of epinephrine (a hormone secreted from the adrenal glands) are increased. I talk more about these hormones and the stress response in Chapter Three, but for now you need to know that this increase in norepinephrine and epinephrine constricts blood vessels; shunts blood from the skin, kidney, and digestive organs to the heart, brain, and skeletal muscles; and raises our heart rate, blood pressure, and blood sugar.
Because gastric emptying is delayed, the oral medications we take are prevented from entering the small intestine and being absorbed. Hence no matter how many pills we swallow, they may not work. Accompanying symptoms to this sympathetic response may include facial pallor, cold hands and feet, chills, nausea and vomiting, diarrhea, restlessness, insomnia, palpitations, dry mouth, headache, light headedness, rapid speech, stuttering, nervousness, irritability, confusion, forgetfulness, anxiety, and panic attacks.
Looking Back and Glimpsing Ahead
In this chapter, you discovered a variety of theories offered by the medical community to explain the cause of migraine disease. You also learned about the role of the sympathetic nervous system in our disorder.
Now that you understand what is happening to your body during a migraine attack, you can apply the knowledge you have gained in the chapters ahead. For example:
You will see how balancing your serotonin levels by avoiding your food and beverage triggers and incorporating integrative therapies like acupuncture, meditation, and exercise into your wellness plan can minimize many of the symptoms you experience during your migraine attack.
You will discover how to curb, or turn off, your sympathetic nervous system and decrease your body's physiologic response to stress, which I talk about in detail in Chapter Three, as well as other chapters throughout the book.
You will have a better grasp of how the medications we look at in Chapter Four can help to relieve, abort, or prevent your headache.CHAPTER 2
Why You Have Migraine Disease
In the introduction, I told you migraine was a genetic, neurological disease. In Chapter One, you looked at the medical theories offered to explain the cause of our disease. Now, you need to examine the genetic relationship.
Although research suggests migraine is a genetically based disease, exact genetics have not been identified. Some sources believe there may be a gene that causes a decrease in serotonin production. Other reports indicate there may be an abnormality in a gene that inhibits the function of a protein called TRESK. TRESK is thought to control nerve cell excitability and the sensation of pain in an area of nerves at the base of the brain (see the "References" section at the end of the book for further information).
While research continues to attempt to link specific genes to the cause of migraines, one thing is known: If one of your parents suffers, or suffered, from migraine disease, there is a fifty percent chance you may as well. Also, the inherited tendency may be passed from another family member, such as a grandparent, aunt, or uncle.
Looking back at my family history, I don't recall either of my parents suffering from migraine disease. However, I have many memories of my father sitting at the dining room table, with his head covered by a towel and his body bent over a bowl of steaming water, trying to relieve the horrible sinus headaches he experienced, which, when I think about it, could have been misdiagnosed. Currently, although I do not have my own children, I have two nieces and a great-nephew who have migraine disease and, like me, started to have the headaches at a young age.
Excerpted from MIGRAINE by Sharron E. Murray. Copyright © 2013 Sharron Murray, MS, RN. Excerpted by permission of Red Wheel/Weiser, LLC.
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