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Conari Press, an imprint of Red Wheel/Weiser, LLC  is the publisher of Sharron's book, Migraine: Identify Your Triggers, Break your Dependence on Medication, Take Back Your Life -  An Integrative Self-Care Plan for Wellness," released June, 2013. Follow Sharron on Twitter @murraysharron, and her page Sharron Murray, MS, RN on Facebook, for tips to help you battle your migraines and achieve wellness.



Do you know the difference between migraine as a headache and migraine as a disease? - Learn about the "Migraine Brain" 




Almost everybody gets a headache sometime in their lives. Because so many people suffer from headaches and headaches have numerous causes, many of which can be life-threatening, the International Headache Society developed a classification system to help doctors provide accurate diagnoses and offer effective treatments for their patients. As well, the specific diagnostic criteria must be fulfilled for patients to be entered into research projects.

The most recent edition of The International Classification of Headache Disorders (ICHD) is the ICHD-3 . The document is extensive. To address its entirety is beyond the scope of this article. Therefore, to give us an idea of the numerous types of headaches a person might experience, we take a brief glimpse at the list of Classifications and Diagnosis. Headache disorders are classified as:

1. Primary: (are caused by independent pathomechanisms)

  • Migraine: including migraine without aura, migraine with aura (aura with headache and aura without headache; migraine with brainstem aura; hemiplegic migraine and types of familial hemiplegic migraine; sporadic hemiplegic migraine; and, retinal migraine), chronic migraine, complications of migraine (Status migrainous, Persistant aura without infarction, Migrainous infarction, Migraine aura-triggered seizure), probable migraine, and episodic syndromes that may be associated with migraine like cyclical vomiting syndrome and abdominal migraine 
  • Tension-type headache: including infrequent episodic, frequent episodic, chronic, and probable
  • Trigeminal autonomic cephalalgias (TACs): including cluster headache, paroxysmal hemicrania, hemicrania continua
  • Other primary headache disorders: including primary cough headache, primary exercise headache, primary thunderclap headache, primary stabbing headache, and new daily persistent headache (NDPH)

 2. Secondary: (a secondary symptom to another disorder known to cause headache)

  • Headache attributed to trauma or injury to the head and/or neck: including head trauma, whiplash, and craniotomy
  • Headache attributed to cranial or cervical vascular  disorder: including ischemic stroke or transient ischemic attack (TIA), intracranial hemorrhage, giant cell arteritis GCA) 
  • Headache attributed to non-vascular intracranial disorder: including increased cerebral spinal fluid pressure, idiopathic intracranial hypertension (IIH), low cerebral spinal fluid pressure, intracranial neoplasm, epileptic seizure
  • Headache attributed to substance or its withdrawal: including carbon monoxide-induced headache, alcohol-induced headache, headache by food or additive (monosodium glutamate-induced headache), cocaine-induced headache, histamine-induced headache, calcitonin gene-related peptide-induced headache, medication-overuse headache (MOH)
  • Headache attributed to infection
  • Headache attributed to disorder of homeostasis: including hypoxia and/or hypercapnia, high altitude headache, airplane travel, driving, sleep apnea, dialysis, pre-eclampsia or eclampsia, hypothyroidism, fasting
  • Headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cervical structure: including cervicogenic, glaucoma, acute and chronic rhinosinusitis, temporomandibular disorder (TMD)
  • Headache attributed to psychiatric disorder

3. Painful cranial neuropathies, other facial pains and other headaches: including trigeminal neuralgia, occipital neuralgia, optic neuritis. 

Keeping these things in mind, it is important for us to know that a person may receive more than one primary headache diagnosis. For example, in my case I have migraine with aura, migraine without aura, and tension-type headache.  As well, we may have a primary headache and receive a diagnosis for a secondary headache such as medication overuse headache or cervicogenic headache. 

Another point to be aware of is that headache is a phase of a migraine attack. A migraine attack is considered to have four phases: premonitory (prodrome), aura, headache, and postdrome (resolution). Not all of us go through each phase. For instance, you may never have an aura. Another person may have an aura without a headache (see ICHD-3 beta, pages 645-650 for specific diagnostic criteria).

In addition, we need to know migraine attacks may be  episodic or chronic. Episodic migraine (EM) includes a range of attack frequency with headache days 0-14 days per month. If our headache days occur on 15 or more days per month (tension-type or migraine-like) for more than 3 months, with the features of migraine headache on at least 8 days per month, we are given the diagnosis chronic migraine (CM). We should know that the most common cause of symptoms of chronic migraine is medication overuse (ICHD-3 beta).

This brings us to a discussion about migraine as a disease.




Migraine is believed to be a genetic neurological disease. As persons with migraine, we are thought to have an inherited sensitivity of the nervous system that makes our brains (neurons) hyperexcitable. This hyperexcitability gives us a predisposition to migraine attacks. Although research continues to explore the exact cause of migraine, a number of areas in our brains are thought to be directly or indirectly involved in the complex pathogenesis, including the hypothalamus, brainstem, cortex, limbic system, and the trigeminovascular pathway (Charles, 2012; Burstein et al., 2015;  Maniyar et al., 2015).

That said, in the Burstein article, during a discussion of disease mechanisms, the authors report, "migraine attacks are likely to begin centrally, in brain areas capable of generating the classical neurological symptoms of prodromes and aura, whereas the headache phase begins with consequential activation of meningeal receptors at the origin of the trigeminovascular system" (p. 6620). Here, it is important for us to know that as a migraine attack progresses through these  phases, a number of electrical and chemical events take place, including the involvement of neurotransmitters, neuropeptides, and proinflammatory mediators such as dopamine, serotonin, norepinephrine, glutamate, nitric oxide, calcitonin gene-related peptide, histamine, bradykinin and protaglandins. The entire range of these mechanisms is thought to be associated with the wide variety of symptoms we experience (Charles, 2012; Burstein, et al., 2015; Maniyar et al., 2015). 

Let's take a brief look at some examples (for more detailed discussions, see references cited):

Premonitory (prodrome) phase: 

Premonitory symptoms may precede the headache phase of a migraine attack, with or without aura. A number of symptoms have been reported, including fatigue, euphoria, depression, irritability, food cravings, constipation, neck stiffness (pain), yawning, difficulties with concentration, nausea, blurred vision, bloating, pallor, change in facial expression or body perception, piloerection, and sensitivity to light, sound, and smell (Charles, 2012; ICHD-3 beta, 2013; Burstein, et al., 2015; Maniyar, et al., 2015). In the Burstein article, the authors report premonitory symptoms most commonly described by patients point to the potential involvement of:

  • the hypothalamus, including symptoms fatigue, depression, irritability food cravings, and yawning;
  • the brainstem, including symptoms muscle tenderness and neck stiffness;
  • the cortex, including symptoms abnormal sensitivity to light, sound, and smell; and
  • the limbic system, including depression and anhedonia (p. 6620). 

In addition, both the Charles and Maniyar articles suggest premonitory symptoms may be associated with the hypothalamus and note the neurotransmitter dopamine may play an important role. In the Maniyar article, the authors also report emotional changes and a feeling of tiredness may result from involvement of limbic/frontal areas mediated by the hypothalamus; posterior hypothalamic dysfunction could explain neck discomfort and stiffness; and, involvement of the frontal cortex could explain difficulties in reading, writing, and concentration (p. 611). It is interesting to note that in the Charles article, the author mentions some premonitory symptoms may come and go before the headache phase, others may build up in intensity leading up to the headache, occur during the headache, and persist well beyond the resolution phase (p.413). 

Aura phase 

Aura may begin before pain, after headache has started, or continue into the headache phase. (ICHD-3 beta, 2013; Maniyar, et al., 2015). In the Burnstein article, the authors report aura symptoms point to the potential involvement of: 

  • the visual cortex, including scintillating lights* and scotomas*;
  • the somatosensory cortex, including paresthesia, and numbness of the face and hands;
  • the motor cortex or basal ganglia, including tremor and unilateral muscle weakness; and
  • the speech area, including difficulty saying words or aphasia (p. 6619). 

*Scintillating lights are visual hallucinations that are bright and fluctuate in intensity. Scotoma is defined as loss of part(s) of the visual field of one or both eyes (ICHD-3 beta, 2013, p. 808).


Headache is usually unilateral, pulsating, moderate to severe intensity, and may be aggravated by movement but may be felt all over the head, (on one or both sides and in the middle of the head), including the eyes, frontal, occipital and neck areas (Kelman, 2005; ICHD-3 beta, 2013; Burstein, et al., 2015). In the Burstein article, the authors report, as headache progresses, we may experience a variety of: 

  • autonomic symptoms, including nausea, vomiting, nasal/sinus congestion, rhinorrhea (runny nose), lacrimation (tearing one or both eyes), ptosis, drooping of upper eyelid) yawning, frequent urination and diarrhea:
  • affective symptoms, including depression and irritability;
  • cognitive symptoms, including attention deficit, difficulty finding words, transient amnesia, reduced ability to navigate in familiar environments; and, 
  • sensory symptoms, including photophobia (sensitivity to light), phonophobia (sensitivity to sound), osmophobia (sensitivity to smell), cutaneous allodynia (sensitivity to touch) and muscle tenderness (pages 6619-6620).


Some symptoms may persist beyond the headache phase. Postdromal symptoms are thought to be similar to those in the premonitory phase and may include: 

  • hyperactivity or hypoactivity (tiredness, weakness, fatigue);
  • cognitive difficulties;
  • mood change (depression);
  • residual head pain, lightheadedness;
  • neck pain and/or stiffness; 
  • yawning;
  • food cravings; and,
  • gastrointestinal symptoms (Charles, 2013; ICHD-3 beta, 2013). 


Numerous sources commonly refer to migraine as a severe headache. However, as the authors of the Burstein article report, the extent of our symptoms suggests that "migraine is more than a headache. It is now viewed as a complex neurological disorder... and as such, it is evident that the migraine brain differs from the nonmigraine brain" (p. 6620).

The authors also mention that "because the migraine brain is extremely sensitive to deviations from homeostasis (wake-sleep cycles, body temperature, food intake, etc.), it seems reasonable that hypothalamic neurons that regulate homeostasis and circadian cycles are at the origin of some of the migraine prodomes" (p. 6629). In line with this, the Maniyar article indicates hypothalamic involvement can explain many of the premonitory symptoms. Here, the authors suggest further research is needed to investigate whether treatment during the premonitory phase can reliably prevent headache in patients who are able to predict the headache phase of a migraine attack (p. 618).

And, lastly, we should know the Charles article reports "a comprehensive approach of migraine demands appreciation of all the phases of an attack and the development of future therapies may hinge not only on an understanding of what goes on in the brain during a headache but also what happens in the hours before it begins and after it ends" (p. 417).


Burstein, R., Noseda, R., & Borsook, (2015). "Migraine: Multiple Processes, Complex Pathophysiology". The Journal of Neuroscience. April;35(17): 6619-6629. 

Charles, A. (2013). "The evolution of a migraine attack - a review of the evidence." Headache. Feb;53(2):413-9. 

Headache Classification Subcommittee of the International Headache Society. The International Headache Society. "The International Classification of Headache Disorders: 3rd edition (beta version). Cephalalgia. 2013;33:629-608. 

Kelman, L. (2005). "Migraine pain location: a tertiary care study of 1283 migraineurs." Headache. Sep;45(8):1038-47.

Maniyar, F. H., Sprenger, T., Monteith, T., et al., (2015). "The premonitory phase of migraine-what can we learn from it?" Headache. May;55(5) 609-20. 

Sharron Murray MS, RN is an author and coauthor CaMEO Study, "Life With Migraine". Currently, Sharron is active in the migraine community as a writer, advocate, American Migraine Foundation Partner, moderator for the American Migraine Foundation "Move Against Migraine" Facebook Group, and member of the National Headache Foundation Patient Leadership Council. 

Follow Sharron on twitter @murraysharron,  her FB page: Sharron Murray, MS, RN 

This article is not intended as a substitute for medical advice. If you have any specific concerns about your health or nutrition, please consult a qualified health care professional.

Updated November 28, 2018

Copyright June 1st, Sharron E Murray, 2016





Migraine: The power of a breath

"Remember to breathe. It is after all, the secret of life." - Gregory Maguire, A Lion Among Men

At birth, we take our first breath. In death, we take our last breath. During the years between birth and death, we may take countless breaths and never think about the 'act of breathing'. That is, until the 'power of a breath' is drawn to our attention.

In my case, the impact of a single breath caught me by surprise my senior year of nursing school. Given all the delivery rooms were full, a classmate and myself had been left to monitor a young, single mother, who was not as far along in her labor as the other mothers. The doctor had been called and, once contractions increased in frequency, we had been instructed to push the emergency bell and alert a registered nurse for assistance. We had also been told, since the baby was going to be given up for adoption, the young mother was not to see her newborn. 

Contractions increased. The bell was pushed. No one came to our rescue. Panic! I was at the foot of the bed and could see the baby's head. Breathless and heart pounding, I grabbed the gloves laid out for the doctor and tried to remember, shoulders down or shoulders up? Guide the baby out. "Oh, God," I still remember my terrified prayer, "Please do not let me drop the baby in the kick bucket."

Meanwhile, my classmate, much calmer than myself, had plopped herself on a stool at the head of the bed, turned on the bit of gas we were allowed to administer, and holding a mask over the young mother's mouth and nose was gently saying, "Breathe in, Breathe out, everything's fine". Amazingly, the rhythm of those words subdued the turmoil inside me. I took a breath, guided the baby out, and, as the doctor and registered nurse entered the room, put the wailing little body on the mother's tummy. The umbilical cord was cut and the newborn was safely transported to the nursery. Sighs of relief.  My classmate had created "calm in the midst of chaos."

Throughout my career in critical care nursing, I used those words to create "calm in the midst of chaos" with patients, families, registered nurses, and student nurses. Depending on the situation, "Breathe in, Breathe out" was followed by "you've got this, everything is under control, I'm here for you", or whatever seemed to be appropriate at the time. Oddly enough, I never applied them to myself and my journey with migraine until my first visit to the migraine clinic. So, now that I have your attention, let's take a closer look at the 'act of breathing" and how, for those of us with migraine, it can help create "calm in the midst of chaos " and, with practice, contribute to a decrease in duration and severity of our migraine attacks.

At this point, we need to be aware that one of the areas in the brain implicated in the pathogenesis of migraine disease is the hypothalamus. The main function of the hypothalamus is to regulate homeostasis, or balance between our internal and external environments.  An example of how the hypothalamus maintains homeostasis, and one that is critical to our survival, is the stress response. The stress response is an adaptive physiological response to a real or perceived threat. When a perceived threat (stressor) is recognized, the hypothalamus tells the adrenal gland to release a flood of hormones, including but not limited to, epinephrine, norepinephrine, and cortisol. For those of us with migraine disease, fluctuations in these hormones may trigger a migraine attack (i.e. "let-down" stress), make us susceptible to other triggers like poor sleep, dehydration, and skipped meals, and given the headache phase of an attack itself may be perceived as a stressor, amplify attack duration and severity. 

Thus, we arrive at the 'power of a breath' and how to create "calm in the midst of chaos". During an attack, along with increased heart rate and blood pressure, our breaths may become rapid and shallow. Only the upper portion of our chest (thorax) may expand, limiting the amount of oxygen that gets to the lower portion of our lungs. Low oxygen levels may make us feel dizzy and lightheaded. Pain and anxiety may make us panic and breathe faster, creating a vicious cycle (chaos). As well, other symptoms we have may be magnified, including cold nose, hands and feet (vasoconstriction); chills; nausea and vomiting; confusion; and, insomnia. In addition, gastric emptying may be delayed (gastric stasis) and the oral medications we take may be prevented from entering the small intestine and being absorbed.

At the migraine clinic, I was told breathing effectively during an attack could help slow my respirations down, increase my oxygen intake, promote relaxation, increase absorption of my medications, and hopefully, decrease the severity and duration of my attack. Made sense to me. In other words, taking my own advice, "Breathe in, Breathe out", I could create "calm in the midst of chaos".

Rhythmic Breathing 

So, let's take a look at a technique, rhythmic breathing, I find particularly helpful (Murray, 2013, p. 153). Most of us are unaware of our breathing pattern, therefore, to begin with, you need to identify your normal pattern of breathing. Place one hand on your chest and the other on your abdomen. Take a breath in and notice which hand moves outward with the breath. If the hand on your chest moved, you are a thoracic (chest) breather. If the hand on your abdomen moved, you are an abdominal breather. You should know thoracic breathing is the usual finding in healthy adult females, and abdominal breathing is predominate in infants, children, adult males (more common with rapid rates) and in the elderly because the chest stiffens with age. (Murray & White, 1999, p.p. 25, 76, 78). The reason females (and perhaps some males) tend to be chest breathers rather than abdominal breathers is not well defined but, in graduate school, I was told it was thought to be related to "vanity" (push the chest out and suck the tummy in).

Rhythmic breathing involves inhaling and exhaling at a fixed pace while you pay attention to the flow of air going in and out of your body. The breath is not forced , and the chest and abdomen move as one unit. On inhalation, this allows the diaphragm to drop down into the tummy and more air to reach the bottom of the lungs. On exhalation, the diaphragm moves back into position, the lungs and respiratory tissue recoil, and air escapes into the atmosphere.  Some sources have you count to 3, 4, or 5 as you inhale and exhale. I have stuck with the words I learned long ago in nursing school, "Breathe in",  and "Breathe out".

So, get comfortable. You can sit or lie down:

  • Place one hand on your lower chest and the other on your abdomen.
  • As you inhale slowly through your nose, say the words, "breathe in".
  • As you exhale slowly through your nose or mouth, say the words, "breathe out".
  • Concentrate on relaxing your muscles.

Slow and and out... a hand on the lower chest and a hand on the belly, everything moving together, expand on inhalation, contract on exhalation. After you repeat the pattern a few times, you should start to feel calm. If you practice this technique throughout the day (standing, sitting, or lying down) between attacks, you will find it easier to draw upon when you have an attack. As well, you may find during any stressful situation or event, you automatically revert to the technique.

"You've got this!" Warm wishes for great success.


Murray, S., MS., RN. Migraine: Identify Your Triggers, Break Your Dependence On Medication, Take Back Your Life.  San Francisco:Conari Press, 2013.

Murray, S. E., MS, RN, &  White, B. S., DrPH, RN-Cs, ANP. GNP. Critical Care Assessment Handbook. Philadelphia: W.B. Saunders Company, 1999.

Sharron Murray MS, RN is an author and coauthor CaMEO Study, "Life With Migraine". Currently, Sharron is active in the migraine community as a writer, advocate, American Migraine Foundation Partner, moderator for the American Migraine Foundation "Move Against Migraine" Facebook Group, and member of the National Headache Foundation Patient Leadership Council. 

Updated November 28, 2018

Copyright May, 2016, Sharron E. Murray.

Follow Sharron on twitter @murraysharron, her FB page: Sharron Murray MS, RN 

This article is not intended as a substitute for medical advice. If you have specific concerns about your health or nutrition, please consult a qualified health care professional.




Can an electronic diary driven by personalized analytics overcome the challenge of identifying and managing individual migraine triggers?  


Although determining migraine triggers is believed to be an important step in migraine management, establishing connections between individual triggers and subsequent attacks is difficult. If you have episodic or chronic migraine and have tried to figure out your triggers, you are probably aware that the process can be a frustrating and stressful event.

Perhaps, the challenge we face is best expressed by Dr. Richard Lipton, a professor of Neurology at Albert Einstein College of Medicine and Director, Montefiore Headache Center, in an article, "Migraine: More than Just a Headache", (Reynolds, 2016). Here is an excerpt:

"Trigger management is very important, but the challenge is that there are huge individual differences in which triggers matter, " says Dr. Lipton. He has seen patients come into his clinic with drastic weight loss because they've tried to avoid every food listed as a potential migraine trigger without knowing if any really affect them personally, "and there's nothing left to eat". True trigger identification, he says, requires that people keep a migraine diary and look at multiple attacks over time.

Dr. Lipton is excited about the new generation of online diary tools, such as N1-Headache (Curelator) , which he recommends to his patients. These tools let people with migraine use a smartphone or tablet to track exposures and symptoms in real time and generate reports of potential triggers they can discuss with their doctor.

"It's one of those areas of medicine where rationalization and individualization is particularly important," says Dr. Lipton, "and the better we get at identifying individual triggers, the better we'll be able to give people individualized advice on trigger avoidance." (p.4/8).

It is important for us to know that in a recent study, "Towards improved migraine management: Determining potential trigger factors in individual patients", (Peris, et al, 2016),  published in Cephalalgia and presented with aditional data at the 58th Annual Scientific Meeting of the American Headache Society, the Headache Group, Department of Neurology at Medical University of Vienna, Austria and Curelator Inc. collaborated in an analytical approach to identify potential trigger-factor associations (potential triggers or premonitory symptoms) with migraine attacks in individuals with migraine. The study authors report individual 'potential trigger' profiles were successfully generated for almost all 326 migraine patients (87%) who kept detailed diaries for 90 days. An average of four trigger factors per patient were associated with an increased risk of attack and in 85% of patients, trigger profiles were highly individual and unique. In an adapted press release, "Triggers for migraine attacks determined for individual patients", (MNT, June 8, 2016), Dr. Christian Wober, one of the study authors and head of the section specializing in headaches at MedUni Vienna's Department of Neurology, is quoted as saying, "For the very first time, this new analysis therefore provides information about the correlation between migraine attacks and a broad spectrum of possible trigger factors for each individual patient and is therefore a step towards personalized migraine management."

This brings us to a discussion about N1-Headache (Curelator) and this new analytical approach to the identification and management of migraine triggers. N1-Headache (Curelator) is a digital tool that guides individuals with migraine to track and discover factors associated with increasing and decreasing the risk of having a migraine attack and dismiss factors that have no effect on attacks. Along with Dr. Richard B. Lipton and Dr. Christian Wober, members of the clinical advisory board are other leading international headache and migraine experts, including  Dr. Peter Goadsby, Dr. Anne MacGregor, Dr. Paul R. Martin, Dr. Noah L. Rosen, and Dr. Stephen D. Silberstein.

People can get N1-Headache (Curelator) at no cost through a coupon referral program that N-1 Headache (Curelator) runs through any participating neurologist (alternatively, a premium version can be purchased on their website). Either way, when a person downloads an app from the N-1 Headache (Curelator) website premium version*, after approximately 90 days of accumulating daily data a subsequent statistical analysis provides the individual three visual maps:

  • Trigger Map (factors showing increased risk of an attack, including high association and low association).
  • Protector Map ( factors associated with a decreased risk of an attack). For example, if poor quality sleep is a trigger for you, good quality sleep may be protective for you; and, if stress is a trigger for you, relaxation may be protective for you.
  • No association Map (factors that do not appear to be associated with an attack). For example, if foods with tryramine show no association with your attacks, there may be no need for you to avoid some of the foods you enjoy.

In addition, you receive a Personal Analytical Report, including the amount of acute medication you have taken (can help identify medication overuse), missed daily medication (preventives), and missed other medications. This report can be shared by you with your physician, or, with your permission, sent to your physician by N1- Headache (Curelator), with the goal of increasing your knowledge of your individual triggers and improving your clinical outcomes. 


I was introduced to N1-Headache (Curelator) in the fall of 2014 and began to use the tool January, 2015. Before starting to use the tool, I, like other users, was asked to list my suspected triggers. It is interesting to note, in a study conducted by N1-Headache (Curelator) of hundreds of individuals analyzed who firmly believed they knew their triggers, the accuracy was surprisingly low. On average, accuracy was less than 20%. Factors accurately identified more frequently than others included stress and sleep quality. Dietary factors did poorly. Two individuals, myself and a person from Northern Europe, had above a 70% accuracy. Both of us had meticulously kept diaries for more than 5 years.

After receiving my first set of trigger maps, I had an interview with Alec Mian, PhD, CEO, N-1 Headache (Curelator). We talked about the method I used to track and successfully manage my triggers, how I use Ni-Headache (Curelator), and my early results. Since that time (almost a year ago), in addition to the information I shared during the interview, I continue to use N1-Headache (Curelator) because:

  • Comorbidities may increase the frequency of migraine attacks and/or headache days. For example, in my situation, I have had comorbid hypothyroidism for decades. About 6 months ago, I noticed an increase in headaches, along with a sluggish digestive system and a general feeling of malaise. My daily diary helped me distinguish between these headache days and migraine (headache phase). After a discussion with my doctor, the dose of my thyroid supplement was increased and the related headaches have diminished. 
  • Following a neck injury in my forties, cervicogenic headache has been, for me, increasingly troublesome. Again, through the data I input, my daily diary helps me distinguish between neck pain associated with cervicogenic headache and neck pain as a premonitory symptom related to migraine. 
  • As I proceed on this journey with trigger management, I find I am able to experiment a bit more with my known triggers. For example, small doses of sun and heat are now tolerable, in particular, if I am relaxed. 
  • Perhaps, most importantly, the few minutes I spend each day punching in my data have become a "mindfulness moment".  A brief time for me to reflect on the challenges of my day, acknowledge emotions like sadness, anger and happiness and let go of what doesn't serve me well. If I feel particularly stressed, I realize I need a session of meditation at bedtime to promote relaxation and help induce sleep. As well, I think about exercise; and, what and how much, I had to eat and drink, not in a stressful way, but one that facilitates learning and reinforces healthy lifestyle habits.


Mian, A. (2015). "Q&A with Sharron Muray and Alec Mian." Curelator Headache. December 3, 2015.

Mian, A. & Martin, P.R. (2016). "Confabulation, card tricks and confirming your migraine triggers (part 1)." Curelator Headache. April 7, 2016.

MNT. (2016). "Triggers for migraine determined for individual patients." Adapted Media Release . Tuesday 7 June, 2016.

Peris, F., Donoghue, S., et al. (2016).  "Towards improved migraine management: Determining potential trigger factors in individual patients". Cephalalgia.  May 14. pii: 0333102416649761 

Reynolds, S. (2016).  "Migraine: More than Just a Headache". A Woman's Health- Women Magazine. April 25, 2016. pp 3-8. 

Sharron Murray MS, RN is an author and coauthor CaMEO Study, "Life With Migraine". Currently, Sharron is active in the migraine community as a writer, advocate, American Migraine Foundation Partner, moderator for the American Migraine Foundation "Move Against Migraine" Facebook Group, and member of the National Headache Foundation Patient Leadership Council. 

Follow Sharron on twitter @murraysharron, her FB page: Sharron Murray, MS, RN 

This article is not intended as a substitute for medical advice. If you have any specific concerns about your health or nutrition, please consult a qualified professional.

Updated November 28, 2018

Copyright, August 4, 2016: Sharron E. Murray 

















The influence of regular lifestyle behaviors in migraine



  "Good habits are worth being fanatical about." John Irving

Much is written about lifestyle habits and migraine. Altered sleep patterns, (poor sleep), hunger (skipped meals, fasting, hypoglycemia), dehydration, high- intensity exercise (strenuous), and stress are thought to trigger migraine attacks. Good quality sleep, regular meals, adequate hydration, low-intensity exercise, and low stress (stress management therapies) are believed to be protective for migraine.

Acknowledging the importance of the role lifestyle factors play in promoting wellness and managing disease, in a recent study, "The impact of regular lifestyle behavior in migraine: a prevalence case-referent study," (Woldeamanuel and Cowan, 2016), the study authors aimed to evaluate the differences in migraine occurrence among participants who do and do not maintain the regular lifestyle behaviors (RLBs) of sleep; exercise; and, daily mealtime pattern and hydration status. Since a review of the literature revealed previous studies have investigated each of these factors alone, the purpose of this present study was to examine the connection between these three factors and migraine occurrence.  In this article we take a look at the authors findings and what the results mean to those of us with migraine. 

To begin with, we should know a bit more about the study. Participants were 175 episodic and 175 chronic migraine patients age 15 years and older, with charts regularly documenting RLB.  Electronic medical records were continuously followed and studied for one year (January 1, 2014 to January 1, 2015) at the "Stanford Headache and Facial Pain Clinic".  Patients younger than 15 years, those with primary insomnia, shift workers, and charts not documenting notes on RLB were excluded. Diagnosis was made using the ICHD-3 beta  (International Classification of Headache Disorders) criteria and each diagnosis was confirmed by a Headache Specialist. The potential for effect modification by medication use (abortive and/or preventive), depression, and anxiety was tallied and analyzed in both episodic and chronic migraineurs. 

The study focused on the following three self-report domains: 

  • Maintaining regular sleep hours with consistent-sleep wake time both in weekdays and weekends.
  • Maintaining regular daily mealtime and adequate hydration status (consisted of keeping consistent meal hours with the number of meals personalized to the preference of each patient as the study focused on regularity of mealtimes rather than frequency); adequate hydration consisted of keeping regular amounts of water intake personalized to patient preference.
  • Maintaining daily aerobic exercise of any form for 20 minutes duration that raised heart rate. 


175 patients with episodic migraine and a combined total of 1016 mean monthly headache days and 175 patients with chronic migraine and a combined total of 3786 mean monthly headache days were continuously enrolled: 

  • In both groups, 22% of the patients were males.
  • The mean age was 41 years in the episodic group and 40 years in the chronic migraine group. 
  • The mean monthly migraine frequency for episodic patients was 5 and 25 among chronic patients.
  • All 3 lifestyle behaviors were seen in lower frequency among the chronic migraine group, with a decreasing pattern from regular mealtime, regular sleep, to daily exercise in both groups. When comparing the impact from each lifestyle behavior to the impact of the combined RLB, regular sleep had identical impact. 
  • The group of chronic migraine patients who followed RLB were progressively converting, month after month, into episodic migraineurs, while episodic migraineurs not following RLB , month after month, were converting into chronic migraine.


It is important for those of us with migraine to know: 

  • The mean age and mean frequency of episodic and chronic migraine were representative of migraine patients in the general population 15 years and older
  • The risk of having chronic migraine was significantly reduced for patients with RLB and higher RLB prevalence was protective from developing chronic migraine.
  • Adjusting these results to the possible effect modifier of medication use and depression and/or anxiety showed no significant implications. 

In addition, along with providing evidence for the importance of sleep regulation in headache medicine, the authors of the study suggest evidence is provided for the relevance of: 

  • Employing non-pharmacological evidence-based migraine therapeutic protocols for individual lifestyle behavior modification that are applicable in daily clinical practice and beyond. 
  • Empowering and reinforcing self-management skills and desirable lifestyle behavior modifications for long-term management and prevention.
  • Behavior modification treatment to help revert and unlearn strategies that led to the formation of undesirable and inappropriate behaviors and teach new and appropriate behaviors. 

Limitations and Conclusions 

The authors conclude engaging in RLB is a moderating factor in migraine. Migraine patients who follow all three domains of RLB are more likely to have episodic than chronic migraine. They add, learning self-regulated behavior can enable the person with migraine form favorable lifestyle habits, which can ultimately help control migraine. The authors suggest the positive results from this study indicate the need for a full prospective randomized controlled clinical trial to further investigate and validate the role and impact of RLB in migraine management. These studies will facilitate investigation into:

  • The degree of flexibility in maintaining RLB.
  • Further validation of causality between lack of RLB and chronic migraine, or whether there is an undetermined factor causing both, e.g. high stress level.
  • The need for psychometrically sound measures or wearable tracking devices to track lifestyle behaviors as they relate to migraine to avoid the limitations of self-report and improve accuracy of real-time data and behavior.

"Strength doesn't come from what you can do. It comes from overcoming the things you once thought you couldn't" - Rikki Rogers 

For many of us with migraine, our attacks may increase in frequency during the busiest years of our lives when we are balancing our jobs, family responsibilities, and social obligations. Maintaining lifestyle habits like regular sleep schedules, mealtimes and hydration, along with daily exercise routines, can be a challenge.

However, we need to be aware that as our attacks increase in frequency, so do a host of other problems that can complicate our treatment and contribute to migraine- related disability. That said, when my migraine attacks escalated from episodic to chronic, making substantial changes in what I ate and drank, my eating and drinking habits, my sleep routine, and learning to manage my physiological  stress response, were the most difficult things I did to reduce the frequency of my attacks and remit from chronic to episodic migraine. But, it is important to note, that as my attacks decreased in frequency, I gained a feeling of empowerment (internal locus of control), which motivated me to continue to create an environment conducive to wellness.

Today, although I have learned to manage my disease and and have infrequent attacks, I continue to  use an electronic tool to track my daily trigger management and to remind myself of the importance of regular lifestyle habits. For me, "Good habits are worth being fanatical about". 


Woldeamanuel, Y. W., & Cowan, R.P. (2016).  "The impact of regular lifestyle behavior in migraine: a prevalence case-referent study." Journal of Neurology. pp 1-8. First online: 25 January.

Sharron Murray MS, RN is an author and coauthor CaMEO Study, "Life With Migraine". Currently, Sharron is active in the migraine community as a writer, advocate, American Migraine Foundation Partner, moderator for the American Migraine Foundation "Move Against Migraine" Facebook Group, and member of the National Headache Foundation Patient Leadership Council. 

Follow Sharron on twitter @murraysharron and on facebook, Sharron Murray, MS, RN

This article is not intended as a substitute for medical advice. If you have any specific concerns about your health or nutrition, please see a qualified health professional.

Updated November 27, 2018

Copyright March 3rd, 2016, Sharron E. Murray 
















Puzzled by migraine triggers? 7 things to know to help manage attacks 

Migraine is believed to be a genetic neurological disease. As persons with migraine, we are thought to have an inherited sensitivity of the nervous system, which makes our brains hyperexcitable. This hyperexcitiability gives us a predisposition to migraine attacks.

Once we have been diagnosed with migraine, we need to know about triggers. Although much is written about triggers and scientific evidence is often insufficient, inconclusive, and debatable, seven important things we should be aware of are:


Triggers are internal and external stimuli that "set off" (provoke, initiate) migraine attacks in those of us who have the disease. In other words, migraine disease makes us vulnerable to triggers. 


It is important for us to know that triggers do not cause our symptoms. "During a migraine attack, a storm of electrical and chemical activity 'switches on' different areas in the brain and surrounding nerves to cause migraine symptoms" (Dr. Andrew Charles, AHS14AZ).


 Triggers thought to be associated with an increased probability of an attack over a brief period of time include: 

  • Altered  sleep patterns (poor sleep, interrupted sleep, oversleeping).
  • Hormonal changes like estrogen withdrawal.
  • Hypoglycemia (missed and skipped meals, fasting).
  • Dehydration.
  • Stress, including perceived emotional stress and "let-down" stress.  As well, stress can make us more susceptible to other triggers. For example, perceived emotional stress may interrupt our sleep or make it difficult for us to fall aseep.
  • Environmental factors like weather changes, bright or flickering lights, loud noises, and strong odors.
  • *Dietary factors including magnesium deficiency and chemicals and additives in foods, such as tyramine (e.g., aged cheeses, bananas, avocados, fava beans, garbanzo beans, lima beans, organ meats like liver, pickled foods, canned soup, nuts, peanut butter, tomatoes, and soy sauce), tannin (e.g., chocolate, cheeses, ice cream, nuts, bananas, smoked foods, and cigarette smoke), aspartame (e.g., diet sodas), phenylethylamine (e.g., chocolate), sulfites (e.g., fermented foods and beverages), nitrites (bacon, ham, pepperoni, and other processed meats), gluten (e.g., wheat, barley, rye, and may be added to number processed foods as thickener,stabilizer, emulsifier, starch, or hydrolyzed plant protein), MSG (e.g., sauces, gravies, processed meas, packaged foods, and canned soups and vegetables).
  • Alcohol.
  • Exposure to, or withdrawal from, certain medications, caffeine.    

*Food cravings (hunger) in the premonitory phase may be mistakenly identified as triggers. For example, declining estrogen levels that occur at the time of menstruation as well as low levels that are encountered during the menopausal transition, are triggers for some women. Low estrogen levels are associated with low serotonin levels. Low serotonin levels may promote food cravings for starches and sugars, including chocolate. If we mistakenly identify a food craving as a trigger, we may unnecessarily avoid something we enjoy.  


While specific triggers may be controversial, in a study where respondents were presented with a list to choose from (Kelman, 2007, cited in Pavlovic et al, 2014), the most commonly occurring triggers were:

  • Stress.
  • Hormones.
  • Missed meals.
  • Weather.
  • Sleep disturbances.
  • Odors.
  • Alcohol.
  • Heat.
  • Foods.


While a single trigger may initiate an attack, a single trigger (apart from menstruation) may not be powerful enough to consistently initiate an attack by itself. In other words, we need to know if a specific trigger is always followed by an attack. Since it may take a combination, or loading of triggers (additive effect, stacking, cumulative) to provoke an attack, it is helpful for us to know which triggers occur either singly or in combination with others. For example, high stress plus poor quality sleep or oversleeping, is associated with an increased chance of an attack. (Spierings et al, (2014)


Perhaps, the most important thing to know about triggers is they are unique to the individual.  Keeping a diary can help us identify our personal triggers and make associations between these triggers and our attacks. An advantage of electronic diaries is they can capture data on the same day and eliminate the inaccuracy of recall, along with the frustration of flipping through pages to try and figure everything out. 


Once we identify our unique triggers, we can avoid or learn to manage them. For example, we can avoid triggers that are not consistent with a healthy lifestyle such as toxic smells; chemicals and additives in foods and beverages; fasting and skipped meals, dehydration; and, lack of sleep or oversleeping.  We can learn to manage others like stress. 


Murray, S. "Can we use associations between migraine triggers, premonitory symptoms, and migraine attacks, to predict our attacks and decrease their frequency?" Sharron Murray's Articles, December, 2014.

Murray, S. , MS, RN. Migraine: Identify Your Triggers, Break Your Dependence On Medication, Take Back Your Life.  San Francisco:Conari Press, 2013.

Sharron Murray MS, RN is an author and coauthor CaMEO Study, "Life With Migraine". Currently, Sharron is active in the migraine community as a writer, advocate, American Migraine Foundation Partner, moderator for the American Migraine Foundation "Move Against Migraine" Facebook Group, and member of the National Headache Foundation Patient Leadership Council. 

Follow Sharron on twitter @murraysharron, her Facebook page: Sharron Murray MS, RN 

This article is not intended as a substitute for medical advice. If you have any specific concerns about your health or nutrition, please consult a qualified health care professional.

Updated November, 2018

Copyright September, 2015, Sharron E, Murray