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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.



Episodic or chronic migraine? How, using scientific-based evidence, we can help our doctors improve our treatment outcomes


"We cannot direct the wind, but we can adjust the  sails." - Bertha Calloway

Migraine, a genetic neurological disease characterized by hyperexcitability and episodic events known as migraine attacks, is classified as a primary headache disorder (ICHD-3). For many of us with migraine, optimal management of our disease is a challenge.

In an important step toward improving our treatment outcomes, a recent study tested the hypothesis that ineffective acute treatment of episodic migraine is associated with new-onset chronic migraine (Lipton, et al., 2015). In line with this approach, authors of a recent article, (Lipton and Silberstein, 2015), discuss how to breakdown barriers to optimal treatment and prevention for those of us with episodic migraine (EM) and chronic migraine (CM).

To help us have a better understanding of the challenges we face and offer suggestions on ways to assist our doctors in improving our treatment outcomes, using information from this study and journal article, this article focuses on our role as patients in:

  • Diagnosis of Migraine. 
  • Diagnostic criteria for Episodic migraine (EM) and chronic migraine (CM).
  • Risk factors for progression to CM.
  • Acute and preventive treatment. 
  • Electronic diaries. 

"The principle of Priority states (a) you must know the difference between what is urgent and what is important, and (b) you must do what's important first." -Steven Pressfield 

Diagnosis of Migraine: 

When we have a severe migraine attack, we want immediate treatment and relief from our headache and associated symptoms. But, to ensure we receive effective treatment, we must have an accurate diagnosis. 

Our diagnosis of migraine is based on a thorough history, including family history and onset of headache; physical examination; and, should they be necessary, diagnostic tests to rule out other headache disorders. To help our doctor make an accurate diagnosis, we need to be familiar with common characteristics of migraine: 

  • for migraine without aura, headache is usually unilateral location, pulsating in quality, of moderate to severe intensity, aggravated by physical activity (need to have at least 2 of the 4 preceding), lasts 4-72 hours without treatment and is associated with at least one of the following: nausea and/or vomiting, sensitivity to light (photophobia), and sensitivity to sound (phonophobia).
  • for migraine with aura, we may have transient focal neurological symptoms that usually precede or may accompany headache, including visual (most common), sensory, speech and/or language, motor, brainstem, or retinal symptoms. Subforms of migraine with aura include: migraine with typical aura (typical aura with headache and typical aura without headache), migraine with brainstem aura, hemiplegic migraine (familial hemiplegic migraine types 1, 2, 3, familial hemiplegic migraine other loci and sporadic hemiplegic migraine), and retinal migraine.
  • premonitory symptoms, (prodromal) which may begin hours or a few days prior to the aura in migraine with aura, and headache in migraine without aura, and continue through to the postdrome. These include stiff neck, neck pain, nause, fatigue, blurred vision, yawning, sensitivity to light and sound, pallor, and difficulty concentrating.

It is important for us to know that we may have: 

  • both migraine without aura and migraine with aura, and
  • migraine with aura without a headache, or with a less distinct headache.

In addition, we need to be aware that frequent episodic tension-type headache often coexists with migraine without aura. Because treatment of migraine differs from that of tension-type headache, we need to be able to distinguish between these two types to help ourselves and our doctors select the right treatment, while avoiding medication overuse (ICHD-3 beta, p. 661). Characteristics of frequent episodic tension-type headache include at least 10 episodes of headache occurring on 14 days or less for >3 months, lasting from 30 minutes to 7 days and, at least two of the following four: 

  • headache typically bilateral location,
  • may be pressing or tightening in quality,
  • is of mild to moderate intensity,
  • does not worsen with routine physical activity.

And, both of the following:

  • headache is not associated with nausea and vomiting, and
  • may be associated with photophobia or phonophobia (only one). 

Diagnostic criteria for EM and CM

EM and CM are differentiated in the number of headache days per month. In EM, headache occurs on less than 15 days per month. If our headaches occur on 15 or more days per month (tension-type-like and/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 of chronic migraine (ICHD-3 beta). We should know that response to triptans is not diagnostic of migraine headache as secondary headaches attributable to other disorders like subarachnoid hemorrhage or meningitis, may respond to triptans (Lipton and Silberstein, p. 106).

About 2.5% of persons with EM progress to CM per year. 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 headache related disability. For example: 

Given this information, along with ensuring an accurate diagnosis for migraine, we need to work with our doctors to set goals and direct our treatment to reducing our attack frequency, as well as determining and treating comorbid disorders. 

Risk factors for progression to CM: 

It is important for us to know that overuse of acute medications, in particular opioids and barbiturates, is a risk factor for progression to chronic migraine and a common cause of chronic migraine symptoms. However, it is difficult to determine whether medication overuse is the cause of or a response to CM (Lipton and Silberstein, 2015). Some of us  revert to EM after medication overuse is stopped, but many of us do not. Patients who overuse opioids are thought to have the highest relapse rate after withdrawal treatment.

Other modifiable risk factors for progression include comorbidities like obesity (2 to 5 times more likely to develop CM than persons normal weight), moderate or severe depression, anxiety, asthma, and allergic rhinitis; snoring; stressful life events; and, caffeine use/misuse (combination medications containing caffeine). Non-modifiable risk factors for progression are thought to include age, female sex, genetics, low education level, low socioeconomic status, and head or neck injury (potentially modifiable).

Once we identify our personal risk factors, our role is  to work with our doctors to improve or eliminate our modifiable ones, decrease the frequency of our attacks, and if we have CM, increase our chances for remission.

"When a lot of remedies are suggested for a disease, that means it cannot be cured." -Anton Chekhov

Acute and Preventive Treatment

Now, let's take a closer look at the study noted at the beginning of this article (Lipton et al., 2015). The authors predicted that poor treatment efficacy among individuals with EM, leading to longer periods of exposure to pain, might increase the risk of new-onset CM. Using the AMPP study survey, respondents identified all medications they used to treat "their most severe type of headaches." For analysis, medications were combined into simple analgesics, combination analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), and triptans. Opioids and barbiturates were combined in one category.

Respondents who used NSAIDs and simple analgesics were less likely to be in the high treatment efficacy categories while persons who used triptans were more likely to be in favorable treatment efficacy categories. The authors note opioids and barbiturates were associated with increased risk of CM in prior studies (Bigal, Serrano et al., 2008).

Results indicated that those with ineffective treatment are at risk for CM onset while those with more effective treatment have better outcomes over 1 year follow-up. The study authors report that these findings support their prediction that exposure to longer periods of pain may be in the causal pathway that leads from EM to CM and suggest that improving treatment outcomes might prevent new onset CM.

If we have EM and a poor response to acute treatment, to decrease the frequency and severity of our attacks, and reduce our chances of progressing to CM, we need to talk to our doctor about acute and preventive treatments as soon as possible. Given individual response to acute therapy varies with the specific drug and dose, and side effects of preventive medications can be unpleasant, to increase responsiveness and compliance, effective communication with our doctor about our progress is essential.

Along with pharmacological treatment and educational interventions, lifestyle modifications and trigger management can help reduce attack-related impairment and decrease the frequency and severity of our attacks. Non-pharmacological approaches for the prevention of EM that have demonstrated efficacy include cognitive behavioral therapy (CBT), relaxation techniques, and biofeedback. These therapies, along with acupuncture, can be used alone or in conjunction with medication (Lipton and Silberstein, 2015).

Electronic Diaries  

One of the most effective ways we can help our doctors improve our treatment outcomes is to keep a diary. Whether a notebook, electronic, or a calendar, a diary can help our doctors and ourselves: 

  • identify possible triggers (trigger patterns) and suggest strategies to minimize or avoid them.
  • recognize premonitory and aura symptoms.
  • recognize the frequency, severity and duration of our migraine attacks (with and without aura, and aura without headache) and headaches (migraine-like and tension-type-like).
  • differentiate tension-type headache from migraine-like headache.
  • identify the location and severity of our pain.
  • assess our functional disability (attack-related impairment).
  • assess the effectiveness of our treatment and recognize the need to adjust doses, alter routes of administration, and add or change our medications.
  • recognize a pattern of medication overuse.
  • assess the effect of lifestyle habits including sleep patterns, skipped meals, exercise, sexual activity, and stress, on the frequency and severity of our attacks.
  • assess the impact of protective factors and nonpharmacological therapies on the frequency and severity of our attacks. 

Given the limitations of paper diaries, including multiple daily entries that have to be made by hand, along with recall bias, in the past few years, electronic diaries have become very popular. However, the authors of a recent review of commercially available mobile apps available in Canada expressed concern about the lack of scientific expertise and evidence base associated with headache diary apps. None of the 38 apps included in their review met all 7 criteria established by the study authors for an ideal diary. Three apps met 5 of the criteria: iHeadache (developed by Better QOL), ecoHeadache (developed by eco TouchMedia), and Headache Diary Pro (developed by Froggyware). Only 18% of the apps were created with scientific or clinical headache expertise. 

An example of a scientific approach to the identification of migraine triggers, as well as to advance basic understanding and management of migraine with the practical intention of reducing suffering and costs associated with the condition, is N1-Headache (developed by Curelator Incorporated). The simple to use app tracks triggers, associations between single or combinations of triggers and the occurrence of migraine headaches (Spierings, Donoghue, et al., 2014). The clinical advisory board includes neurologists and headache specialists active in clinical practice and research. "Although initial clinical trials have ended, Curelator Headache will constantly run a cohort 1000-2000 patients in clinical trial." (Interview with Alec Mian, CEO at Curelator, March 5th, 2015).


Bigal, M.E., Serrano, D., Buse, D., et al. (2008). "Acute migraine medications and evolution from episodic to chronic migraine: a longitudinal population based study." Headache.  48:1157-1168.

Buse, D.C., Silberstein, S.D., et al. (2013). "Psychiatric comorbidities of episodic and chronic migraine." J Neurol.  Aug;260(8):1960-9. DOI 10.1007/s00415-012-6725-x. 

Headache Classification Subcommittee of the International Headache Society. The International Headache Society. "The International Classification of Headache Disorders: 3rd edition (beta version). Cephalalgia.  2013;33:629-808.

Hundrert, A.S., Huguet, A., et al. (2014). "Commercially available mobile phone headache diary apps: a systematic review." JMIR Mhealth Uhealth.  Aug 19;2(3):e36 doi: 10.2196/mhealth.3452.

Lipton, R.B., Fanning, K., et al. (2015). "Ineffective acute treatment of episodic migraine is associated with new-onset chronic migraine." Neurology. Jan 21. doi: 10.1212/WNL.0000000000001256.

Lipton, R.B., Serrano, D., et al. (2014). "Sociodemographic, Disability, and Employment Differences Between Persons With Chronic and Episodic Migraine: Results of the CaMEO (Chronic Migraine Epidemiology & Outcomes) study." Neurology. April 8, vol. 82 no. 10. Supplement S41.002.

Lipton,  R.B., & Silberstein S.D. (2015). "Episodic and Chronic Migraine Headache: Breaking Down Barriers to Optimal Treatment and Prevention." Headache: The Journal of Head and Face Pain. Volume 55, Issue Supplement S2. DOI: 10.1111/head.12505_2.

Spierings, E.L., Donoghue, S., et al. (2014). "Sufficiency and necessity in migraine: how do we figure out if triggers are absolute or partial and, if partial, additive or potentiating? Oct;18(10):455. doi: 10.1007/s11916-014-0455-y.

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 Facebookpage: 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, March 24, 2015: Sharron E. Murray




Migraine, "Sinus" headaches and "Sinusitis" - Facts we need to know


                     "A correct diagnosis is three-fourths the remedy." - M.K. Gandhi 

Several studies and reports indicate that migraine is often misdiagnosed by ourselves or our physicians as sinus headache or sinusitis. In a recent study designed to estimate the frequency of misdiagnosis of sinusitis among migraine patients (Al-Hashel et al., 2013) results showed: 

  • of 130 migraine patients who met the ICHD-III-beta criteria (International Classification of Headache Disorders, 3rd edition), 106 patients were misdiagnosed as sinusitis.
  • the delay in diagnosis ranged from 1-38 years.
  • chronic migraine was significantly higher in misdiagnosed patients compared to patients with the correct diagnosis.
  • medication overuse headache (MOH) was reported only in patients misdiagnosed as sinusitis.
  • a delay in the diagnosis of migraine led to chronification of the headache and transformation, in some cases, into MOH. 

The authors propose that the delay in diagnosis could be attributed to the presence of sinus pain, sinus congestion, and nasal discharge during headache attacks. They go on to say that these autonomic symptoms have been reported in previous studies which concluded the "presence of autonomic symptoms during migraine attacks often leads to confusion and incorrect diagnosis of sinusitis." They add, "appropriate recognition of migraine in patients who complain about sinus headaches may help to minimize the suffering and unnecessary interventions, start migraine directed therapy, and improve quality of life".

Therefore, to increase our knowledge about "sinus" headache, "sinusitis" and migraine, and help us receive appropriate diagnosis and treatment, this article addresses:

  • what is "sinus" headache?
  • what is "sinusitis"?
  • how to differentiate "sinusitis" from migraine.
  • can "sinusitis " trigger a migraine? 

What is "sinus" headache? 

Sinus headache is commonly thought of as pain and pressure in the forehead, behind the eyes, or in the face, but may be referred posteriorly. The areas are tender to touch and the headache is often accompanied by: 

  • nasal and sinus congestion,
  • clear nasal discharge, and 
  • watery eyes.

We should know that the ICHD-III-beta criteria states that "the term 'sinus headache' is outmoded because it has been applied both to primary headaches (migraine and tension-type) and headaches supposedly attributed to various conditions involving nasal or sinus structures."  The previously used term "sinus headache' has been replaced with "Headache attributed to disorder of the nose or paranasal sinuses" and is associated with other symptoms and/or clinical signs of the disorder. 

What is "sinusitis"? 

True sinus headache is more properly called "sinusitis" or rhinosinusitis (Cady, 2008, and Hutchinson, 2011). It is often associated with viral or bacterial infection and may be characterized by:

  • purulent (thick yellow or green) nasal discharge,
  • decreased smell and taste,
  • bad breath,
  • fever,
  • cough, (may be productive of mucous and worse at night),
  • general feeling of illness (malaise), 
  • pain and pressure in our upper teeth, forehead, behind our eyes and in our face, and
  • pain may worsen when we lean forward or bend our heads.

The pain should improve with remission of a viral infection (within 7days) or, if our infection is bacterial, successful treatment with antibiotics. With persistent or recurrent infection, we may have to undergo a CT scan or nasal endoscopy to rule out signs of obstruction, polyps or other signs of sinus disease.

We should know the ICHD-III-beta criteria says, "simply finding pathological changes on imaging of acute rhinosinusitis, correlating with the patient's pain description, is not enough to secure the diagnosis of acute rhinosinusitis. Evidence of causation should be demonstrated by at least two of the following: 

  1. headache has developed in temporal relation to the onset of the rhinosiusitis
  2. either or both of the following: headache has significantly worsened in parallel with worsening of the rhinosinusitis; headache has significantly improved or resolved in parallel with improvement in or resolution of the rhinosinusitis
  3. headache is exacerbated by pressure applied over the paranasal sinuses
  4. in the case of unilateral rhinosinusitis, headache is localized ipsilateral to it."

How to differentiate sinusitis from migraine:

According to the ICHD-III-beta criteria, the presence or absence of purulent discharge and other features of acute rhinosinusitis help differentiate these conditions. Or, in the words of Dr. Susan Hutchinson (2011),  "in the absence of fever, pus from your nose, alteration in smell or foul smelling breath, you likely have a migraine headache".

Dr. Hutchinson suggests an additional way to determine whether our headaches are migraine is to ask ourselves the following questions taken from Dr. Richard Lipton of Einstein College of Medicine ID Migraine Questionnaire:

  •  In the last 3 months, how disabling are your headaches; do they interfere with your ability to function? (Are you missing work; school; family activities?)
  • Are your headaches ever associated with nausea? 
  • Are your headaches ever associated with sensitivity to light?

If we meet two of the three above criteria, migraine is likely present 93% of the time. When all three are present, migraine is likely 98% of the time.

Dr. Hutchinson adds, "your diagnosis needs health practitioner confirmation for accuracy and best treatment. She goes on to say "getting the right diagnosis and treatment can free you from the recurring burden of failed headache treatment and disability".

Can sinusitis trigger a migraine? 

According to ICHD-III-beta criteria, an episode of migraine may be triggered or exacerbated by nasal or sinus pathology. Dr. R. Cady, (2008), explains this as, "People with migraine inherit a nervous system that is more sensitive to change than those without migraine. If the nervous system perceives a threat from either the external or internal environment, the nervous system response can be an attack of migraine."

Every addition to true knowledge is an addition to human power."- Horace Mann   

In my situation, I was misdiagnosed with sinus headache for a number of years. Like many patients, I went through a number of failed treatments, including over the counter and prescription decongestants, antihistamines, nasal sprays, analgesics, and anti-inflammatory medications, before I went to a migraine clinic and was told my symptoms were part of my migraine.

However, along with migraine disease, I can still have an episode of acute rhinosinusitis. To help prevent the rhinosinusitis from triggering or exacerbating a migraine attack, I monitor other internal and external trigger factors that might increase the probability of an attack and, where possible, initiate protective factors (Lipton et al., 2014 and Pavlovic et al., 2014). These include:

  • Stay hydrated as mouth breathing and fever can lead to dehydration. Drinking plenty of fluids also helps keep mucous thin.
  • Eat regular meals or, if my appetite is poor, 6 small meals a day to avoid hunger.
  • Avoid dairy products as increase mucous.
  • Maintain a regular sleep routine to avoid altered sleep patterns. This is sometimes difficult because night time cough, snoring, and sinus pressure, along with a dry mouth may inhibit sleep. A humidifier is helpful to increase moisture in my room. A glass of water by my bedside helps with dry mouth.  
  • Consult with my doctor if I need medication to relieve my symptoms.
  • Monitor my stress levels and use techniques like meditation and biofeedback to help me relax (quiet my mind and calm my body).

In summary: 

  • migraine is commonly misdiagnosed as sinus headache.
  • sinus headaches are more properly called rhinosinusitis .
  • rhinosinusitis is associated with purulent nasal discharge.
  • migraine may be associated with watery eyes and runny nose, but the fluid is clear.
  • patients with rhinosinusitis may also have migraine.
  • rhinosinusitis may trigger or exacerbate a migraine attack.
  • see your doctor for a full diagnosis for your headaches as treatment of rhinosinusitis differs significantly from treatment for migraine (Cady, R., 2008, and Hutchinson, S., 2011).



Al-Hashel, J., Y., Ahmed, S., F., Alroughani, R., & Goadsby, P., J. (2013). "Migraine misdiagnosis as a sinusitis, a delay that can last for many years." The Journal of Headache and Pain. 14:97. doi: 10.1186/1129-2377-14-97.

Cady, R., K., MD. (2008). "Sinus Headaches, Allergies, Asthma and Migraine: More Than a Causal Relationship?" Headache, The Newsletter of ACHE. Summer 2001, Volume 12, Issue 2. Updated November, 2008. 

Eross, E., Dodick, D., & Eross, M. (2007). "The Sinus, Allergy and Migraine Study (SAMS)." Headache. Feb;47(2):213-24.  

Hutchinson, S., MD. (2011). "'Sinus Headache'"or Migraine". Headache, The Newsletter of ACHE.   

International Classification Committee of the International Headache Society (IHS). "The International Classification of Headache Disorders, 3rd edition (beta version)". Cephalalgia.  33(9) 764-765 (629-808).

Lipton, R., B., Pavlovic, J., M., Haut, S., R., Grosberg, B., M., & Buse, D., C. (2014). "Methodological Issues In Studying Trigger Factors and Premonitory Features of Migraine." Headache. Nov;54(10):1661-9. doi:10.1111/head.12464. Epub 2014 Oct 23.

Pavlovic, J., M., Buse, D., C., Sollars, M.,Haut, S., & Lipton, R., B. (2014). "Trigger Factors and Premonitory Features of Migraine Attacks: Summary of Studies." Headache. Nov;54(10):1670-9. doi:10.1111/head.12468.

Schreiber, C., P., Hutchinson, S., Webster, C., J., Ames, M., Richardson, M.,S., Powers, C. (2004). "Prevalence of migraine in patients with a history of self-reported or physicain-diagnosed "sinus" headache." Arch Inter Med. Sep 13;164(16):1769-72.

Sharron is a health and wellness author. A migraineur herself, her most recent book, "Migraine: Identify Your Triggers, Break Your Dependence On Medication, Take Back Your Life-An Integrative Self-Care Plan For Wellness", (2013), is a Conari Press Publication.

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

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 professional. 




Can we use associations between migraine triggers, premonitory symptoms, and migraine attacks to predict our attacks and decrease their frequency? 


"The world is full of suffering. It is also full of overcoming it." -Helen Keller 

For many of us with migraine, our world revolves around painful and debilitating attacks. Addressing this issue, the authors of two recent journal articles have drawn attention to how, if knowledge and understanding of relationships between trigger factors, protective factors, and premonitory features can be established, we may be able to improve our ability to predict, preempt, and reduce the frequency of these acute episodes (Lipton et al., 2014, and Pavlovic et al., 2014).

In this article, we use these journal articles, and the definitions provided within them, to guide us in a discussion of: 

  • trigger factors,
  • protective factors,
  • premonitory features, 
  • self-prediction, and 
  • preemptive therapy. 

Trigger Factors

Before we get to trigger factors, let's review a bit about migraine. Migraine is a neurological disease. As migraineurs, we are thought to have an inherited sensitivity of the nervous system that makes our brains hyper-excitable. This hyper-excitability gives us a predisposition to migraine attacks. 

Attacks, including headaches and other symptoms, are referred to as the ictal state. The goal of treatment in the ictal state is to relieve pain and restore function. The time between attacks, where we may be relatively free of symptoms but have a predisposition to attacks, is referred to as the inter-ictal state. The goal of treatment in the inter-ictal state is to reduce the probability of transitioning to the ictal state. 

Now, let's examine trigger factors. Triggers are internal or external stimuli that provoke or "set off" migraine attacks in those of us who have the disease. 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 of our brain and surrounding nerves to cause migraine symptoms" (Dr. Andrew Charles, AHS14AZ).

As well, we need to be aware that triggers are different from risk factors. Risk factors like genetics, sex, and obesity, increase the onset of the disease in a person previously free of migraine. 

That said, Lipton et al., (2014), define trigger factors as measurable endogenous (internal) or exogenous (external) events (exposures) associated with an increased probability of an attack over a brief period of time.

Endogenous trigger factors include:

  • altered sleep patterns.
  • hormonal changes like estrogen withdrawal.
  • hypoglycemia (skipped meals, fasting).
  • hyperglycemia (blood sugar spikes).
  • dehydration.
  • psychological factors such as stress or relaxation following stress.

Exogenous trigger factors include: 

  • environmental factors like weather changes, bright or flickering lights, loud noises, and strong odors.
  • dietary factors.
  • alcohol.
  • exposure to, or withdrawal from, certain medications.

To help us understand how these triggers can increase the probability of an attack over a brief period of time, let's take a look at observations from a 28-day study of 33 patients with chronic migraine and 22 patients with chronic tension-type headache. The objective was to evaluate the time-series relationships between stress, sleep duration, and headache pain (Houle et al., 2012, cited in Spierings et al., 2014).

Observations for the stress-headache relationship are:

  • High stress yesterday and today predicts very high headache activity today.
  • Low stress yesterday and today predicts low headache activity today.
  • Low stress yesterday and high stress today also predicts low headache activity today.
  • High stress yesterday and low stress today predicts high headache activity today.

The conclusion is that headache precipitation needs at least 2 consecutive days of stress and that it is more likely to occur during let-down stress. Let-down stress was confirmed in a study by Lipton et al., (2014).

Observations for sleep duration and headache are: 

  • Low sleep duration (<4 hours) yesterday and today predicts very high headache activity today.
  • Low sleep duration yesterday and high sleep duration today also predicts high headache activity today.
  • Approximately 8 hours of sleep on consecutive days predicts low headache activity today. 

The conclusion is that headache precipitation needs at least 2 consecutive days of sleep deprivation and that headache is likely to occur with oversleeping.

Observations for stress and sleep duration are: 

  • Low stress and low sleep duration are associated with the lowest headache activity today.
  • High stress and high sleep duration are associated with the most headache activity today.  

Protective factors: 

While trigger factors increase the probability of a migraine attack, protective factors are events that decrease the probability of attacks over a defined period of time (Lipton et al., 2014). Keeping the above observations in mind, the protective factors would be low stress and high quality sleep (8 hours). Other examples include: eating regular meals, practicing relaxation techniques, and preventive medications. Also, we should be aware that things which make us feel better can decrease the length and severity of our symptoms. Examples include: cold packs, sleep, and for some, Essential Oils and aromatherapy .  

Premonitory features (Prodrome)

Premonitory features are defined as subjective cognitive, behavioral, or physical features that precede the onset of aura in migraine with aura, and before the onset of pain in migraine without aura (Lipton et al., 2014, and  Pavlovic et al., 2014). These symptoms may begin within 2-48 hours (some suggest 72 hours as symptoms may develop slowly) of aura or headache onset. Premonitory symptoms may include:

  • fatigue (feeling tired, weary),
  • hunger (change in appetite),
  • food cravings,
  • yawning,
  • difficulty concentrating, thinking, reading, and writing,
  • dizziness,
  • irritability (mood changes),
  • stiff neck,
  • neck pain,
  • light sensitivity,
  • blurred vision,
  • noise sensitivity,
  • sensitive skin,
  • pallor,
  • nausea, 
  • constipation,
  • frequent urination,  
  • thirst, and
  • lots of energy.

About one third of patients with migraine seen in headache centers have premonitory symptoms (Lipton et al., 2014). For those of us who have premonitory symptoms (prodrome), it is interesting to note that in a study of 893 patients (Kelman, 2004), where one third of the participants had prodrome symptoms, the most common symptoms were tiredness, mood changes, and gastrointestinal symptoms.  As well, results showed patients with prodrome differed from patients without prodrome in having more triggers, longer duration of aura and  longer time between aura and headache; more aura with no headache; longer time to peak headache and to respond to triptan; longer duration of headache; more headache associated nausea, running of nose and tearing of eyes; and, more and longer duration of postdrome (resolution phase).   


Self-prediction refers to our assessment of the probability that we will have a migraine attack over a defined period of time (Lipton et al., 2014). To predict our attacks we need to be familiar with our trigger factors and premonitory symptoms and be able to associate them with headache onset. Finding these associations can be challenging.

Let's take a look at some of the challenges we may face:


To begin with, because most of the literature regarding migraine triggers consists of studies performed using patient interviews and surveys, the results may be subject to recall bias and selection bias. With a lack of sound scientific evidence to support our beliefs that a certain trigger initiates an attack, a number of our triggers come under scrutiny.  

For example, many people claim they are 'better than the weatherman" in predicting the weather. However, several studies suggest that our perception of weather as a trigger may be overestimated (Friedman and De Ver Dye, 2009).  This appears to be true for a number of other environmental influences, such as indoor and outdoor lighting, poor air quality, noise, and exposure to strong odors and chemicals (including those in foods and beverages), even though we are believed to be more sensitive to various environmental stimuli than individuals without migraine. 

Unique to the individual 

While specific triggers may be controversial, a vast number of studies show we have a wide range of these precipitating factors. In one of the largest studies to date, when asked, about triggers, 76% of 1750 individuals with ICHD-2 diagnosis of migraine reported triggers. When presented with a list of triggers to choose from, this figure rose to 95% (Kelman, 2007, cited in Pavlovic et al., 2014)). The most common triggers, occurring at least occasionally, were: 

  • stress (80%), 
  • hormones (65% of women),
  • missed meals (57%), 
  • weather (53%0,
  • sleep disturbances (50%),
  • odors (44%).
  • alcohol (38%),
  • heat (30%), and 
  • foods (27%).  

In the Kelman study, we need to know that those of us with triggers were shown to have more severe attacks and symptoms, higher recurrence rates, more associated sleep and mood disturbances, longer lifetime duration of migraine, and more family members with migraine. In addition, migraine with aura and chronic migraine were more frequently associated with triggers than migraine without aura and episodic migraine.


In this instance we need to know if a specific trigger is always followed by an attack. In a study of 120 patients with migraine or tension-type headache (Wober et al., 2006, cited in Spierings et al., 2014), participants were asked if triggers brought on their headaches always (consistently), or sometimes (occasionally). Of the fifteen most common triggers acknowledged (menstruation, weather, stress, red wine, smoking, hunger, alcohol, skipping meals, noise, change in sleep habits, glare, relaxation after stress, exhaustion, odors, and physical activity), only menstruation was statistically significant as a constant rather than occasional trigger.


This brings us to the inference that single triggers (apart from menses) might not be consistently potent enough to initiate an attack and therefore it may take a combination of triggers (additive effect). For example, we discussed the relationship between sleep and stress. Other examples include stress and hunger, (Turner et al., 2013), and combinations of chemicals in foods and beverages, such as tannin, tyramine, and MSG.     

Mistaken identity 

Here, those of us with premonitory symptoms need to know that, in this phase, we may mistakenly identify triggers or confuse them with premonitory symptoms. For example, many of us believe chocolate is a trigger for our attacks. However, consider hormonal migraines. Declining estrogen levels that occur at the time of menstruation as well as low levels that are encountered during the menopausal transition are migraine triggers for some women. Low estrogen levels are associated with low serotonin levels. Low serotonin levels promote food cravings for starches and sugars, including chocolate. If we regularly eat chocolate during these times, we may be experiencing a chocolate craving as a premonitory feature, not a trigger factor.

Fatigue (exhaustion) is another confusing factor. Feeling tired or weary is recognized as  a trigger, a premonitory symptom, and a feeling of exhaustion that persists through an attack and hangs on for days. Extreme fatigue may be a symptom of chronic stress.   

The way to find a needle in a haystack is to sit down -Beryl Markham    

To help us make associations between triggers, premonitory symptoms, and attacks, which can be like trying to find "needles in a haystack", we are encouraged to keep diaries. In other words we need to "sit down" and record a large amount of data. 

If we are using paper diaries, our recall ability, combined with the chore of flipping through pages to try and figure things out, may make us frustrated, especially if our attacks are high frequency or chronic. Hence, we may give up.

In my case, I opted out of paper diaries and journals and initially used a bank calendar, then my Day-Timer (a monthly calendar I could see at a glance). Appointments, work commitments, social obligations, family responsibilities, etc. were already scheduled in. All I had to do was make a note of perceived triggers, including, stress, what I ate or drank, environmental influences like weather, noise and light, hormonal influences, sleep patterns, and premonitory symptoms, along with medications, protective factors and comfort measures that helped me find relief.

Since then, options for diaries have expanded with technological advances. Data can be captured within the same day and time stamped to eliminate the frustration and inaccuracy of recall. In a large electronic diary study, where patients were asked how likely they were to have a migraine, a close relationship between the estimated probability and observed probability showed 72% accuracy (Giffin et al., 2003, cited in Lipton et al, 2014).)

"You can't stop the waves but you can learn to surf." -Jon-Kabat-Zinn (Amaal Starling MD AHS14AZ)

Once trigger factors are identified, we can avoid or learn to mange them.  For example, we can avoid triggers that are not consistent with a healthy lifestyle such as toxic smells, hunger, dehydration, and lack of sleep. We can learn to manage, "learn to cope" (train ourselves not to over-react to stimuli), with other triggers like  stress (Martin et al., (2014).

Recognizing our premonitory symptoms as signs of an impending attack gives us a window of opportunity to intervene with protective factors.  For example, in my case, fatigue, blurred vision and irritability are definite indications that a headache phase is on its' way. Since I have become accomplished at protective measures such as biofeedback, diaphragmatic breathing, and meditation, I can often take action to avoid, or lessen, the pain and associated symptoms (ictal state).

Preemptive therapy 

Preemptive therapy (or short term prophylactic treatment) is an emerging strategy with features of both acute and preventive treatment (Pavlovic et al., 2014). The advantage for people who spend most of their time in the inter-ictal state and are able to reliably predict attacks is that medication may be taken only when it is needed, that is in advance of an anticipated attack to avoid a headache, not on a daily basis (Lipton et al, 2014). An example of this approach is the short-term prevention of menstrual migraine. An additional advantage is that, because medication is taken only when necessary, it reduces exposure to medication and the harmful effects of medication overuse.

"Life is 10% what happens to you and 90% how you can handle what happens to you." -Anonymous 

There is no cure for migraine disease. However, as research continues to progress, we can increase our knowledge and understanding of associations between trigger factors, protective factors, premonitory features and attacks, and improve our ability to predict attacks , as well as decrease their frequency.



Friedman, D., I., MD., MPH., & De Ver Dye, T., PhD. (2009). "Migraine and the Environment." Headache. Feb;25:941-950.

Kelman, L. (2004). "The premonitory symptoms (prodrome): a tertiary care study of 893 migraineurs." Headache. Oct;44(9):865-72. 

Lipton, R., B., Pavlovic, J.,M., Haut, S. R., Grosberg, B. M., and Buse, D., C. (2014). " Methodological Issues In Studying Trigger Factors and Premonitory Features of Migraine". Headache. Nov;54(10):1661-9. doi:10.1111/head.12464. Epub 2014 Oct 23. 

Martin, P., R., & Reece, J., et al. (2014). "Behavioral management of the triggers of recurrent headache: A randomized controlled trial." Behavioral Research and Therapy. 61: 1-11.    

Pavlovic, J., M., Buse, D., C., Sollars, M., Haut, S., & Lipton, R., B. (2014). "Trigger Factors and Premonitory Features of Migraine Attacks: Summary of  Studies." Headache.  Nov;54(10):1670-9. doi:10.1111/head.12468.   

Spierings, E., L., H., Donoghue., S., Mian, A., & Wober, C. (2014). " Sufficiency and Necessity in Migraine: How do we Figure Out if Triggers are Absolute or Partial and, if Partial, Additive or Potentiating?" Curr Pain Headache Rep. 18:455. DOI. 1007/s11916-014-0455-y.  

Turner, D., P., et al. (2014). "Nightime snacking, stress, and migraine activity." J Clin Neurosci.  

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.

Copyright December, 2014, Sharron E. Murray

Updated February, 2019










Migraine-15 steps to create an environment conducive to wellness

"Things may happen around you, and things may happen to you, but the only things that really count are the things that happen in you." -Eric Butterworth   

Migraine is a complex neurological disease. As persons with migraine, we are thought to have an inherited (genetic) sensitivity of the nervous system that makes our brains (neurons) hyperexcitable. Because we have sensitive nervous systems, we are vulnerable to changes in our internal and external environments. 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. 

There is no cure for migraine. However, an environment conducive to wellness can flourish when balance and harmony exist within ourselves (internal environment) and our surroundings (external environment); in other words, with homeostasis. Constructive steps I learned when my migraines were chronic and I had medication overuse headaches, and that help me thrive today, include:

  1. Identify, manage and, where possible, eliminate your personal triggers.  For example, chemicals and additives in foods and beverages, environmental factors, hormones, magnesium deficiency, and alterations in our physical and emotional states. Maintaining a daily diary can make the task easier, as well as provide a wealth of information for you to share with your doctor.
  2. If the task of identifying your individual food and beverage triggers seems overwhelming, it may help you to begin by eliminating the most popular like alcohol, caffeine (exposure to or withdrawal from), fast food, junk food, sodas, and anything with additives, preservatives, MSG, pesticides, and nitrites. Keep in mind that sweet (including chocolate), rich, salty, and fatty foods may be cravings we experience in a prodrome (premonitory symptoms) and may be mistaken for a trigger. In addition, many of these may contribute to development of comorbid disorders like hypertension, stroke, heart disease, and obesity. As well, some of them put us at risk for the development of type 2 diabetes.
  3. While avoiding your individual triggers, eat a healthy diet (organic, if possible) of fresh fruits and vegetables (lots of green, leafy), whole grains, fish, chicken and smaller amounts of dairy and red meat to help keep serotonin and magnesium levels in balance (low serotonin and magnesium levels are linked to migraine attacks).
  4. Establish regular meal times as highs (hyperglycemia) and lows (hypoglycemia) in blood sugar can trigger an attack.
  5. Avoid fasting as hypoglycemia can trigger an attack.
  6. Stay hydrated as dehydration can trigger an attack.
  7. Avoid environmental pollutants and toxins whenever you can.
  8. Use medications, herbs, and supplements under the guidance of your physician or other health care practitioner and follow directions to avoid toxic reactions and medication overuse headaches.
  9. Maintain a regular sleep schedule and avoid stimulants like caffeine (up to 6 hours), and alcohol and electronic devices at least 2 hours before bedtime. Altered sleep patterns (poor sleep quality) may trigger an attack.
  10. Correct bad posture and reduce the strain on muscles in your neck and shoulders.
  11. Check with your doctor and then begin a moderate exercise program to maintain serotonin levels.
  12. Learn to balance your emotions and control your physiological response to perceived stressors through techniques like self-awareness, cognitive behavioral therapy, daily meditation, biofeedback, guided imagery, and similar focused-breathing techniques.
  13. Incorporate other integrative therapies such as acupuncture, mind-body exercises like tai chi and yoga, reflexology, healing touch, massage, and/or Reiki into your wellness plan to promote relaxation.
  14. If you are an overachiever, learn to set priorities, delegate, say "no", and keep a balance in your daily schedule so one activity does not impose on another.
  15. As much as possible, maintain a positive attitude (on my rough days, it helped me to think of something that made me smile). Positive thoughts have been shown to boost our immune system and contribute to wellness.

Focusing on my good days gave me strength to make it through my bad days and as the good days began to outnumber the bad days, I gained the motivation I needed to succeed. Warm wishes for the best possible wellness for you.

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 specific concerns about your health or nutrition, please contact a qualified professional.

Updated February, 2019

Copyright 2014, Sharron E. Murray





Risk of high frequency migraine increases by 40-60% during perimenopause and menopause - "Are you ready for the ride of your life?" -What you need to know 

"Do not become alarmed when you experience yourself in totally new ways," sighs Grandmother Growth, tenderly. "You are changing, getting ready to be initiated into the third stage of your life. Are you ready for the ride of your life? -Susan Weed, Menopausal Years the Wise Woman Way

Menopause marks a major life transition for women, an end to our reproductive years and the cessation of menses. While the end to menstruation and the fear of an unwanted pregnancy may be welcomed by some, others may experience a sense of loss as their last opportunity for conception disappears. Many women may have concerns about cognition and memory, mood disorders, weight gain, increased signs of aging like wrinkles, curtailed sexuality, and decreased libido.

For those of us with migraine, "the ride of our lives" may come with additional challenges. A new study reported at the 56th Annual Scientific Meeting of the American Headache Society found the risk of high frequency migraine attacks increases by 40-60% during perimenopause and menopause for some women.

Data from the 2006 American Migraine Prevalence and Prevention (AMPP) Study survey was used for the analysis (Poster Presentation, Martin et al, 56th Annual Scientific Meeting of the AHS, 2014):

  • Women between ages 35-65 years who met the modified ICHD-3 beta criteria for migraine were included.
  • Women who had never menstruated, were pregnant, breast feeding or using exogenous sex hormones were excluded. Other exclusions included polycystic ovarian syndrome, hysterectomy, or oophorectomy.
  • Women with migraine were classified into a high frequency group if they experienced 10 or more headache days per month and into a low or moderate frequency migraine group if they had less than 10 headache days per month based on responses to the Migraine Disability Assessment Scale (MIDAS).
  • Women were classified as premenopausal (regular menstrual cycles without variation in cycle length), perimenopausal (cycle lengths varied by 7 or more days or periods of amenorrhea lasting 2-11 months) and postmenopausal (absent menstrual periods for at least 12 months) based upon responses to the questionnaire.
  • Women also completed the Patient Health Questionnaire Depression module (PHQ-9) and 3) and Allodynia Symptom Checklist-12 (ASC-12).  

The study authors conclusions were as follows:

  • To our knowledge, ours is the first study to demonstrate that high frequency headache is increased by 40-60% in women during the perimenopause and postmenopause compared to the premenopause.
  • The effect of the menopause and postmenopause on headache frequency is robust to adjustment by depression and allodynia.
  • The strongest predictor of high frequency headache was depression, with odds of high frequency headache being 131% higher for those with depression than without.
  • It is quite likely that the changes in ovarian hormones that occur during the perimenopause and the early postmenopause trigger headaches in these women.

"Persistance in scientific research leads to what I call instinct for truth." -Louis Pasteur

In a press release from the  AHS, Dr. Martin, study lead author, is quoted as saying, "These results validate the belief by many women that their headaches worsen during the transition into menopause." He adds, "We hope our work spurs researchers to develop novel treatments for migraine during this period given that many of the headaches encountered are thought to be hormonally triggered." Dr. Richard Lipton, study co-author adds, "We believe that both declining estrogen levels that occur at the time of menstruation as well as low levels that are encountered during the menopause are triggers of migraine in some women."

To appreciate the significance of the results and conclusions in this study, as well as the implications these findings have for our unique journeys with migraine, this article addresses:

  • the influence of estrogen on migraine.
  • depression and migraine.
  • association of allodynia in migraine with mood disorders and other chronic pain conditions.
  • perimenopause, menopause and migraine.

The influence of estrogen on migraine

Although the association between estrogen and migraine warrants further research, some of the explanations of how estrogen influences migraine that we need to be aware of include:

  • Genetic predisposition (MacGregor, 2010, Sacco et al, 2012). 
  • Estrogens may interfere with cellular excitability (MacGregor, 2009, Sacco et al, 2012). 
  • Estrogen is thought to influence the pain pathway associated with migraine by binding to its receptors on the trigeminal nerves. The trigeminovascular system consists of a network of cranial vessels and their trigeminal innervations that convey pain information to the central nervous system where pain is perceived. The pain response increases by the release of vasodilating neuropeptides especially calcitonin gene-related peptide-CGRP (Milan, 2012, and Sacco et al, 2012).
  • There is an interrelationship between estrogen and brain neurotransmitters, including serotonin, dopamine, norepinephrine, and endorphins. In particular, estrogen is believed to have a potent effect on the serotonergic system (Sacco et al, 2012).
  • Estrogen is associated with increased production of serotonin, reduced serotonin reuptake and decreased serotonin degradation (MacGregor, 2010).
  • Low serotonin levels have been linked to migraine.
  • Because serotonin enhances endorphins (natural analgesic found in the gray matter of the brain), low levels can increase sensitivity to pain. 

Depression and migraine

At this point, it is helpful for us to take a quick look at serotonin. Serotonin is a neurotransmitter in our brain important for managing mood, appetite, sleep and dreaming. For example, high levels make make us feel full, calm, relaxed and even drowsy. Low levels may cause us to feel anxious, irritable and depressed. 

Given the strongest predictor of high frequency headache in this study was depression, we need to know that several studies have linked migraine with mood and anxiety disorders. Some studies suggest mood and anxiety disorders are 2-10 times more prevalent among persons with migraine (comorbid) than in the general population. As well, increased migraine frequency (chronic migraine) is associated with higher rates of depression. (Buse et al, 2012). It has been suggested:

  • serotonergic and dopaminergic dysfunction underlies the comorbidity of depression and migraine (Buse et al, 2012), and
  • "conditions that are comorbid with migraine such as depression and anxiety have presumptive serotonergic mechanisms "(Shapiro, 2008, p 29).

Keeping these things in mind, we also need to be aware that a recent study on "Depression in women: windows of vulnerability and new insights into the link between estrogen and serotonin", (Lokuge, 2011), suggests the effects of estrogen on serotonin may have implications on female mood disorders such as premenstrual disorders and depression during pregnancy, postpartum, and during the menopausal transition.

Association of alloydynia in migraine with mood disorders and other chronic pain conditions

Now, let's peek at cutaneous allodynia (CA). CA is thought to be a result of central nervous system sensitization, which makes us hyperresponsive to otherwise innocuous tactile stimuli. For example, it may hurt to brush our hair or try to put it into a ponytail. As an attack progresses, we may experience sensitivity on extracranial locations such as the arm (Shapiro, 2008, p. 30).  Here, we should be aware that in an estimation of the prevalence and severity of  CA in headache sufferers, results of the AMPP Study (2008) showed CA was more common among migraineurs with female sex, high attack frequency, increased body mass index, disability and depression. 

That said, in a study examining the relationship of migraine with comorbid mood disorders and other chronic pain conditions, (Tietjen et al, 2009), results demonstrated symptoms of CA in migraine were associated with current anxiety, depression, and several chronic pain conditions, including irritable bowel syndrome, fibromyalgia and chronic fatigue syndrome.   

Peri-menopause, menopause and migraine

Holding on to what we have learned so far, it's time to review some general information about perimenopause, menopause, and migraine. To begin with, let's take a brief look at what happens to every women during perimenopause and menopause.

We need to know that as we age and enter perimenopause, our ovaries lose their ability to undergo ovulation and produce estrogen and progesterone. Our pituitary gland, via the hypothalamic-pituitary-ovarian axis, attempts to compensate by releasing follicle-stimulating hormone (FSH) to stimulate an ovarian follicle to produce estrogen. Transient increases of estrogen can occur during this time as FSH surges to stimulate remaining follicles. Menstrual irregularities occur, with sometimes prolonged and heavy menstruation mixed with periods of amenorrhea. When no more follicles remain for stimulation, estrogen levels dramatically decline and menstruation ceases.

Approximately 75-80% of women experience perimenopausal and menopausal symptoms.  Sources vary, but, in general, symptoms are thought to emerge up to 4 years prior to cessation of menses (perimenopause) and may persist for several years postmenopause. Symptoms are believed to be related to the withdrawal of estrogen. Many of them are thought to be associated with resultant changes in the central nervous system neurotransmitters, including serotonin, dopamine and norepinephrine.; and, serum electrolytes, including calcium, magnesium, sodium and potassium. They include:

  • Vasomotor disturbances ("hot flashes", "night sweats"). Although the exact cause is not known, vasomotor disturbances are believed to be caused by a narrowing of the thermoneutral zone in the brain related to the central nervous system neurotransmitters (Archer et al, 2011). In other words "our thermostat is broken". The feeling of intense heat that begins in our upper chest or neck, proceeds up to our face and head and may spread throughout our body, can last for several seconds or minutes and be accompanied by profuse perspiration. When "hot flashes" occur at night, they interrupt our sleep (insomnia). We need to know that they can be precipitated by heat, alcohol, spicy foods, and stress.
  • Sleep impairment.
  • Fatigue.
  • Depression, irritability and other mood disturbances.
  • Cognitive difficulties (loss of concentration, poor memory).
  • Weight gain. Numerous factors may be involved, including decreased metabolism; decreased serotonin levels, with resultant increase in food cravings; and, increased sympathetic nervous system activity, with resultant fluctuation in hormones like cortisol. It is important for us to know that weight gain during this period is often associated with fat deposit in the abdomen, which can increase our risk for developing insulin resistance, diabetes, hypertension and heart disease. Hypothyroidism may become prevalent and exacerbate symptoms like fatigue, weight gain, and mood changes.
  • Sexual dysfunction, including decreased libido.
  • Urinary incontinence.
  • Musculoskeletal pain.
  • Osteoporesis.

Now, let's relate these symptoms to migraine. As you can see, many of these symptoms are the same as (and may be easy to confuse with and exacerbate) migraine triggers (e.g., sleep impairment and fatigue), migraine symptoms (e.g. cognitive difficulties, musculoskeletal pain), and comorbidities (e.g. depression and anxiety).

To add to our discomfort, perimenopause and menopause are the very busiest years of our lives. Many of us are juggling family and career responsibilities, or perhaps, financial worries about college for our children and retirement for ourselves and our partners. The added stress can contribute to migraine as a trigger and a factor that makes us more susceptible to all of our triggers. When chronic, stress can deplete our estrogen levels, decrease our serotonin levels, increase anxiety and depression, and increase the frequency of our attacks. In addition, chronic stress may precipitate an earlier perimenopause and menopause.

"Are you ready for the ride of your life"?

Given I went through a surgical menopause at the age of 42 because of an ovarian cancer scare, I was not prepared for the "ride of my life". Twelve years later, I was diagnosed with chronic migraine, accompanied by medication overuse headaches.

Acknowledging surgical menopause has more severe consequences, to help you prepare and "cushion your ride" through a natural perimenopause and menopause, along with an accurate diagnosis for migraine, it would seem appropriate for you to know where you sit in the menopausal transition:

  • "Despite the increased prevalence of headache and migraine in women in their 40s, migraine is underdiagnosed in this population" (MacGregor, 2009).
  • If you have symptoms suggestive of perimenopause and menopause, along with headaches and other symptoms of migraine, it is important to talk to your doctor about all of your symptoms so they can be managed effectively, with the potential to reduce progression to chronic migraine, comorbidities like depression, unpleasant symptoms such as allodynia, and resultant disability. Blood tests to measure FSH and estrogen levels can determine where you are at in the menopausal transition.
  • The lack of an accurate diagnosis for migraine has been shown to be a barrier to our care,  which may include pharmacological and non-pharmacological interventions. (Buse. et al, 2014).

That said, while we wait for novel treatments to emerge, current pharmacological and non-pharmacological  management of migraine in perimenopause and menopause addresses the same issues as management of migraine at any time, with perhaps the addition of hormone replacement therapy (HRT) at the lowest dose possible to maintain a stable estrogen environment (MacGregor, 2012). It is important for you to know that the benefits and risks of HRT vary with the individual and warrant a thorough discussion with your physician.

In  conclusion, keep in mind our migraine brain likes peace and harmony (homeostasis). Avoiding your other migraine triggers, maintaining a healthy diet and lifestyle habits, and participating in a regular exercise program, along with stress management strategies like mind-body and relaxation techniques, and other modalities like acupuncture, can help you decrease the influence of perimenopause and menopause on your migraine attacks, take control of your attacks and, as I do now, assist you to live a happy and healthy third stage of your life, with migraine.

Sharron :)


American Headache Society. "Women With Migraine Experience More Headaches During The Menopausal Transition: Results From The American Migraine Prevalence And Prevention (AMPP) Study." Press Release: Wednesday, June 25, 2014, !2:01 a.m. EDT

Archer, D. F., Sturdee, D. W., et al (2011). "Menopausal hot flushes and night sweats: where are we now?" Climateric.  Oct 14;(5):515-28 doi: 10.3109/13697137.2011.608596. 

Bigal, M. E., Ashina, S., et al (2008). "Prevalence and characteristics of allodynia in headache sufferers: a population study. Neurology. Apr 22;70(17):1525-33. doi: 10.12/01.wnl.000031064

Buse, D. C., Silberstein, S. D., et al (2013). "Psychiatric comorbidities of episodic and chronic migrane." J. Neurol. Aug;260(8):1960-9. doi: 10.1007/s00415-012-6725-x.

Buse, D. C., Lipton, R., et al (2014). "Barriers to Chronic Migraine Care: Results of the CaMEO (Chronic Migraine Epidemiology & Outcomes) study." Poster presented at the 66th Annual Academy of Neurology Annual Scientific Meeting, Philadelphia, PA. April26-May 3.

Edyta, J. Frackiewicz, N. R., Cutler. (2000). "Women's Health Care During the Perimenopause." J Am Pharm Assoc. 40(6).  

Lanje, M. A., Dr., Bhutey, A. K., Dr. et al (2010). "Serum Electrolytes During Different Phases of Menstrual Cycle." International Journal of Pharma Sciences and Research.  Vol.1(10), 435-437. ISSN: 0975-9492.

Lokuge, S., Frey, B. N., et al (2011). "Depression in women: windows of vulnerability and new insights into the link between estrogen and serotonin." J Clin Psychiatry.  Nov;73(11):e1563-9. doi: 10.4088/JCP.11com07089.  

MacGregor, E. A. (2009). "Estrogen replacement and migraine." Maturitas. May 20;63(1):51-5. doi: 10.1016/j.maturitas.2009.03.016.   

MacGregor, E. A. (2009). "Migraine Headache in perimenopausal and menopausal women. " CurrPain Headache Rep. Oct;13(5):399-403.

MacGregor, E. A. (2010). "Menstrual Migraine: Therapeutic Approaches." Ther Adv Neurol Disord.  May;3(3):197.

MacGregor, E. A. (2012). "Perimenopaual migraine in women with vasomotor symptoms." Maturitas. Jan;71(1):79-82. doi: 1016/j.maturitas.2011.11.001.

Martin, V. T., Pavlovic, M. J., et al (2014). "The menopausal transition is associated with higher headache frequencies in women with migraine: Results from the American Migraine Prevalence and Prevention (AMPP) Study." Poster presented at the 56th Annual Meeting of the American Headache Society. Los Angeles, CA. June 25-29th. 

Milan, A., Puri, V., Puri, S., PhD.(2012). "Effects of estrogen on the serotonergic system and calcitonin gene-related peptide in trigeminal ganglia of rats." Ann Neurosci. Oct;19(4): 151-157. doi: 10.5214/ans.0972.7531.190403.

Murray, S., M.S., R.N. Migraine: Identify Your Triggers, Break Your Dependence on Medication, Take Back Your Life-An Integrative Self-Care Plan For Wellness. San Francisco: Conari Press, 2013.

Sacco, S., Ricci, S. et al (2012). "Migraine in women: the role of hormones and their impact on vascular diseases." J Headache Pain. Apr;13(3): 177-189. doi: 10.1007/s10194-012-0424-y.

Shapiro, R. E. (2008). "Pathophysiology and Genetics of Migraine and Cluster Headache." In M. Levin (Ed.), Comprehensive Review of Headache Medicine. (pp 21-32). New York: Oxford University Press.

Tietjen, G. E., Brandes, J. L., et al (2009). Allodynia in migraine: association with comorbid conditions." Headache. Oct;49(9): 13333-44. doi: 10.1111/j.1526-4610.2009.01521.x.

Sharron is a health and wellness author. A person with migraines herself, her most recent book is, "Migraine..."

Follow Sharron on twitter @murraysharron, her Facebook page SharronMurray, MS, RN, and her website

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

Copyright, October: 2014, Sharron E. Murray