Migraine: The Definitive Guide to Understanding and Managing Severe Headaches

By Britt Talley Daniel MD

A Comprehensive Resource for Migraine Sufferers With a Level of Detail to Satisfy Medical Professionals

This second edition of

• Language: English
• Publisher: Britt Talley Daniel
• Release date: Jan 1, 2024
• ISBN: 9798892389044

Book preview

CHAPTER 1

MIGRAINE WITHOUT AURA

The doctor went to the front lobby, picked up a chart, and called the name of the next patient. A red-haired woman dressed in pants and a designer blouse stood up and came in. He watched her walk to his office and offered her a seat on the sofa. He sat across from her in a comfortable leather chair, holding a pen and a notebook in his lap.

Tell me what brings you in today, the doctor said matter-of-factly.

My headaches,’ she replied, looking up from her lap quickly. I used to get them once or twice a year, but lately …"

The patient paused for reflection and took a deep breath. She looked down again and then up at the doctor who waited patiently.

Lately, they’ve been more frequent, she said with a sigh. And intense.

Do you have more than one kind of headache, the doctor asked.

No, just this same one that keeps coming time and again, the woman answered.

Would you please describe a typical headache then? the doctor asked. Take me through from beginning to end.

Sometimes I can tell one is going to come on before the pain starts. It’s hard to describe but I feel elated, or I have a lot of energy or something like that. This occurs hours to half a day before the headache starts. Then usually they start right here, behind my right eye.

He watched her put her right index finger over her right eye.

There it feels like a white-hot poker or a needle; sometimes it throbs or feels like someone is trying to push my eyeball out.

Anything else? the doctor asked.

Well, that’s usually it, but sometimes they start in the back of my neck. Then after an hour or so the pain comes over my head and locates behind my right eye just like I told you.

Then is that headache just like the first one you told me about? the doctor asked.

Yes, pretty much. They just start differently, the patient replied.

How frequent are your headaches? the doctor asked. On a monthly basis?

Usually 3 or 4 per month, if it’s a good month. Five sometimes if they’re bad, the patient replied.

What’s the duration of your headaches? the doctor asked.

It used to be that I’d take 2 Excedrin Extra Strength and lie down for an hour and my headache would go away in 3 or 4 hours. Then when I got my first job, working as a teller at a bank, my headaches returned. They would last all day if they started in the morning, or half the day if they came on over lunch, and sometimes they would still be there the second day, although usually diminished somewhat, but not always. I have a headache 3 or 4 times a month, and especially before my period starts, the patient stated.

Do you have a headache a few days before or after your monthly flow starts? the doctor asked.

Yes, usually the day before I start and those are the worst ones, the patient said.

The worst? the doctor asked.

Yes, more severe, more nausea. I go to bed, the patient replied.

How long have you had that many per month? the doctor asked.

Too long for me, the patient said, shaking her head and running her hand through her hair. But to answer your question, I would say for about a year or so.

She spoke to the doctor plaintively, I want them to stop.

I know you do and we’re going to work on that, the doctor said measuredly. Although I would like you to consider treating, rather than curing, the headaches. What would you say is the duration of a typical headache?

Usually all day, until I go to bed at least and then sometimes the next day too, the patient answered.

Would that be 24 hours, 36 hours? the doctor asked.

I’d say 36 hours usually, although every now and then I have a real whopper that lasts 3 days, the patient replied.

Are the headaches throbbing? the doctor asked.

Yes, real head bangers. I can hear my heart in my head. It throbs. It pulses. I just want to wrap something cold and tight around my head. The patient said.

On a scale of 1 to 10 for grading headache pain intensity, where 10 is the worst, what would be a number that would fit your headaches? the doctor asked.

Ten plus! the patient said, rising up on the couch and leaning forward with emphasis.

Do you have any associated symptoms with your headaches? the doctor asked. You know, like nausea or vomiting?

They make me sick, but I rarely vomit, the patient replied. I want to shun the light and sounds are amplified like crazy. My daughter crying, when she was young, would drive me crazy. I want to be in a quiet, dark room.

Some persons find that odors or movement make their headaches worse. Does that ring any bells? the doctor asked.

We had to move rooms in a hotel once, and boy, was my husband mad—because we asked for a smoke-free room and the minute I walked in there, I could smell it: dry, days-old cigarette smoke. I got an immediate migraine, and I had my husband call to change us to another room, which thankfully he did, the patient said dramatically.

What about movement? Does that make your headaches worse? the doctor asked. Some people find that exercise, climbing stairs, housework, or even just being upright makes their headaches worse. Does any of that sound familiar to you?

Yes, that’s me. In the bed for the rest of the day, the patient replied.

So, this describes your headaches then? You don’t have any other types? the doctor asked.

Pretty much, the patient responded.

Do you get tension-type headaches? You know the kind where your temples or your neck feels tight. Headaches that come in response to stress, the doctor asked.

Well, yes. I thought everybody had headaches like that, the patient sheepishly admitted.

Do you carry tension in your neck, shoulders, or back? the doctor asked.

Yes! Every day, but that’s just normal. I can live with that, the patient replied.

Do you ever medicate those milder headaches? the doctor asked.

No, not usually. Well, that’s not true. Sometimes I take Extra Strength Tylenol for those, and it helps, the patient added.

What about for the more severe headaches, what do you take for those? the doctor asked.

Extra Strength Excedrin, 2 at the onset and 2 to 4 later at 2-hour intervals, the patient replied.

How well does Excedrin work? the doctor asked.

The patient shrugged and held up her hands palms up.

I wouldn’t be here if what I took worked, would I? the patient answered shrewdly.

Of course not, the doctor replied.

Really the best thing that works is just to go to bed. If I can get to sleep, I usually wake up in a few hours and the headache is gone, the patient said.

Do you get ‘sinus headaches’? the doctor asked.

Yes, sometimes. Those are located over or below my eyes and they are not too severe. I can usually get rid of them with Tylenol Sinus medication.

With a sinus headache do you have a nasal discharge? the doctor asked.

Sometimes I have a clear sinus discharge, but most of the time it’s just that my nose is stopped up and I can’t breathe. My eyes water and it feels like pressure in my sinuses, the patient said.

I have some quick yes/no type of headache questions, the doctor said. Does anyone in your family have headache?

My mother does and her mother, and oh, my sister has ‘sinus headaches’ too, the patient replied.

What about motion sickness, nausea with driving in the car or on a boat?

I’ve had that all my life, and my daughter does too, although as I get older it doesn’t seem so bad, the patient said.

What about hungry headaches?

I get those, the patient said.

Do you get nocturnal headaches that occur in the middle of the night and wake you up for no reason? the doctor asked.

Sometimes I get a headache about 4 am and then I go back to sleep, but when I get up the next morning—watch out, it’ll be a doozy, the patient said.

What about headaches that come if you get hot, like being in the sun or working out? the doctor asked.

I get those sometimes, the patient said.

Do you get headaches when you are stressed or when you are free from stress, like on a weekend, vacation, or holiday? the doctor asked.

I do, the patient replied. A lot of Sundays are ruined by my headaches, and I had a killer headache last Christmas.

Do you get headaches from something cold on the roof of your palate—ice cream or brain freeze headaches? the doctor asked.

Yes, the patient replied.

Do you get headaches from any foods or wines, things that you eat or drink? the doctor asked.

Red wine will give me a headache within 30 minutes, the patient said. And chocolate does too, which is unfortunate because I love chocolate.

You already mentioned that you get headaches that come around your menstrual cycle, the doctor commented. Did you ever take the birth control pill, and did it have any effect on headaches?

I took the pill for 6 weeks and started getting very frequent headaches, the patient replied. My gynecologist took me off them and told me I couldn’t take them.

Do you get headaches when the barometric pressure changes, like when the weather changes? the doctor asked.

Yes, and I get them with mountain sickness when I go skiing in Colorado, the patient replied.

"When you get one of these headaches, which I am going to call migraine without aura, do you experience any trouble with vision, like before the headaches start?" the doctor asked.

Trouble with vision? the patient wondered.

Seeing spots, or holes, or half of things, or a crystal-like object with jagged flashing edges that move? the doctor asked.

No, I haven’t had that, the patient replied. but I thought headache with those symptoms were really what one called ‘migraine.’

The most prevalent type of migraine is migraine without aura, which is much like the headaches you describe, the doctor said. Well, that concludes what I wanted to ask you at the start of the interview, the doctor said. Next I want to do a neurologic exam and then we’ll talk some more.

International Classification of Headache Disorders ICHD-3

In International Classification of Headache Disorders ICHD-3, migraine without aura has the following characteristics⁶:

A. 5 attacks fulfilling B to D.

B. attacks lasting 4 to72 hours

C. at least 2 of the following:

unilateral location

pulsating quality

moderate or severe intensity-prohibits or inhibits daily activities

aggravation by walking stairs or similar routine activity

D. at least one of the following:

nausea and/or vomiting

photophobia and phonophobia

E. history, physical, neurological examinations do not suggest disorders in groups 5 to 11 of IHS classification

General statements about migraine without aura

Doctors are taught patterns of illness. Over 90% of clinical diagnosis is the doctor’s active act of listening to the patient’s symptoms, asking the right questions, and then assimilating what has been learned into a diagnostic formulation. All of this applies to migraine.

The definition of migraine that I am going to discuss next is a modern expression of what migraine is now considered to be. In chapter 6, when the history of migraine is discussed, one may see how far have evolved our concepts regarding what causes migraine. The definition of migraine that I am going to offer is, in my lifetime, a new understanding. It is not what I was taught when I had my first lectures on headache, in medical school in the late 1960s.

Many of my lectures on headache then centered on the vasodilating theory of migraine, as proposed by John Graham and Harold Wolff in 1938.⁷ In those days, a tension-type headache was called muscle contraction headache and migraine was thought to be caused solely by vasodilation of cerebral arteries.

But the thinking about these conditions changed. Part of the change in the thinking about migraine came from work by Professor JW Lance at the Neurology Department at the University of New South Wales in Sydney, Australia. Dr Lance proposed his theory regarding A neural origin for migraine in Neuro View Trends in Clinical Neurology. I still have my handwritten notes from a lecture dated September 26, 1984, when Dr Lance discussed his new theory at a lecture for grand rounds at the University of Texas Southwestern Medical School in Dallas.

He wrote a provocative article in Neurology in 1993 titled, Current concepts of migraine pathogenesis, in which he laid down the basis for the new, changed theory for migraine.⁸

Migraine is a neurovascular reaction to sudden changes in the internal or external environment. Each individual has a hereditary migrainous threshold, with the degree of susceptibility depending on the balance between excitation and inhibition at various levels of the nervous system.

The mechanism of migraine has been presented as an unstable trigeminovascular reflex with a segmental defect in the pain control pathway. This defect permits excessive discharge of part of the spinal nucleus of the trigeminal nerve and its thalamic connections in response to excessive discharge of part of the spinal nucleus of the trigeminal nerve and its thalamic connections in response to excessive afferent input or corticobulbar drive. The end result is the interaction of brain stem and cranial blood vessels, with the afferent impulses from the latter creating the throbbing (pulsating) character of the headache.

Diffuse projections from the locus ceruleus to the cerebral cortex could initiate cortical oligemia and possibly spreading depression. Activity in this system could account for the migrainous aura that may occur quite independently of the headache.

Dr Lance said that his explanation of the cause of migraine was speculative but plausible. In time it has become the new dogma.

Whereas in the past, head pain was thought to originate from tension in scalp and neck muscles or dilatation of blood vessels, neither of these theories has gained scientific support. Therefore, central nervous system mechanisms of headache pain are of current interest. The aura of migraine headache is thought to be similar to a spreading wave of electrical depression moving over the occipital cortex. Dilation and constriction of cerebral arteries occurs, as does a phase of release of inflammatory vasoactive neuropeptides.

Migraine researcher PJ Goadsby, previously of the Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, UK, has researched pain mechanisms in the brains of experimental animals.⁹ Recently he proposed that dopaminergic mechanisms may be involved in control of normal trigeminal information. Dr Goadsby correlates activity in the periaqueductal (PAG) gray area of the brain with migraine. For instance, activation of the PAG makes experimental animals quiet; they don’t want to move, but mainly sit in their cages—much like persons in the midst of a migraine. Dr Goadsby said,

The fundamental problem they (migraine patients) seem to have, as far as I can see, is a dishabituation—an aminergic, sensory dishabituation—the burden of which seems to fall on the brain stem and its manifestation falls broadly on the nervous system."

Definition of migraine

Migraine is a genetic, inherited condition involving the brain, the trigeminal nerve, and cranial blood vessels. It consists of symptoms of episodic headache with intervening periods of normal health. Writing in 2002 in The New England Journal of Medicine in an article titled, Migraine: current understanding and treatment, PJ Goadsby, RB Lipton, and MD Ferrari, stated,¹⁰

Migraine is characterized by episodes of head pain that is often throbbing and frequently unilateral and may be severe. In migraine without aura (previously known as common migraine), attacks are usually associated with nausea, vomiting, or sensitivity to light, sound, or movement.¹¹

When untreated, these attacks typically last 4-72 hours.¹² A combination of features is required for the diagnosis, but not all features are present in every attack or in every patient. These symptoms distinguish migraine from tension-type headache, the most common form of primary headache, which is characterized by the lack of associated features. Any severe and recurrent headache is most likely to be a form of migraine and to be responsive to antimigraine therapy.¹³

In 15% of patients, migraine attacks are usually preceded or accompanied by transient focal neurologic symptoms, which are usually visual; such patients have migraine with aura (previously known as classic migraine).¹⁴ In a recent large, population-based study, 64% of patients with migraine had only migraine without aura, 18% had only migraine with aura, and 13% had both types of migraine (the remaining 5% had aura without headache). Thus, up to 31% of patients with migraine have aura on some occasions,¹⁵ but clinicians who rely on the presence of aura for the diagnosis of migraine will miss many cases.

R Hargreaves and SL Shepheard writing in 1999 in the Canadian Journal of Neurologic Science on Pathophysiology of migraine: new insights stated,¹⁶

Current theories propose that the primary dysfunction in migraine occurs within the CNS [central nervous system] and that this evokes changes in blood vessels within pain-producing intracranial meningeal structures that give rise to headache pain.

Migraine is now thought of as a neurovascular disorder.

It has been proposed that genetic abnormalities may be responsible for altering the response threshold to migraine specific trigger factors in the brain of a migraineur compared to a normal individual.

The exact nature of the central dysfunction that is produced in migraineurs is still not clear and may involve spreading depression-like phenomena and activation of brainstem monoaminergic nuclei that are part of the central autonomic, vascular and pain control centers. It is generally thought that local vasodilation of intracranial extracerebral blood vessels and a consequent stimulation of surrounding trigeminal sensory nervous pain pathways is a key mechanism underlying the generation of the pain associated with migraine.

This activation of the trigeminal vascular system is thought to cause the release of vasoactive sensory neuropeptides, especially CGRP [calcitonin gene-related peptide], that increase the pain response. The activated trigeminal nerves convey nociceptive information to central neurons in the brainstem trigeminal sensory nuclei that in turn relay the pain signals to higher centers where headache pain is perceived. It has been hypothesized that these central neurons may become sensitized as a migraine attack progresses.

Rami Burstein, writing in 2001 in Pain on Deconstructing migraine headache into peripheral and central sensitization, stated,¹⁷

Migraine is a recurring neurological disorder commonly known as a throbbing unilateral head pain that is readily aggravated by routine physical activities. But the clinical definition of migraine includes a host of neurological symptoms other than pain, namely, nausea, photophobia, phonophobia, osmophobia, fatigue, and numerous disturbances in autonomic, mental, sensory, and motor functions.

The neural mechanisms underlying the development of migraine attacks are poorly understood. An attack can be precipitated by a wide variety of internal and external factors, including hormonal changes, psychosocial stress, certain foods, hunger, lack of sleep, excessive sleep, as well as by visual, auditory, olfactory, or somatosensory stimulation.

The potential of any of these factors to trigger a migraine attack appears to vary through complex interactions with the physiological milieu and individual genetic predisposition. For example, migraine attacks are more likely to develop during certain phases of the menstrual cycle (i.e., ovulation, menstruation), during certain phases of the sleep cycle (e.g., upon waking up), or in association with hunger.

In general, 70% of headaches are tension-type headache, 30% of headaches are migraine, and less than 1% of headaches are something else, such as acute bacterial sinusitis, a brain tumor, or some other organic type of headache.

In the clinical interview at the start of this chapter the patient fits the pattern of migraine without aura. In general, 70% of migraines are migraine without aura and 30% are migraine with aura. Many patients who lack the typical visual symptoms of migraine with aura doubt they have a diagnosis of migraine, perhaps because of the media’s stress on visual aura type symptoms.

Migraine is familial in occurrence and about 80% of patients who have migraine will have someone in their family with it. The problem here is accurate diagnosis and many patients will state their mother had sinus headache not knowing that these may really be migraine. The clinical historian has to be vigilant and inquire about the gamut of pseudo names migraine may be called to get the history straight.

Migraine occurs in women about 3 times as often as in men.¹⁸ Studies of the US population have revealed about 30 million American migraine sufferers, with a female to male ratio of 3:1.

The prevalence of migraine in the US is one person with migraine for every 4 households. Migraine is a disabling condition and is more prevalent than diabetes and asthma combined.

About 18% of the US population of women has migraine, while 6% of men have it.¹⁹ Patients with migraine are generally first seen by their primary care doctor. The median pain intensity of a migraine attack is said to be 8 on a scale of 1-10 and the median duration of an attack is 18 to 24 hours.²⁰

About a third of patients with migraine miss at least 1 day of work every 3 months. Migraine is said to be the most common chronic human health problem for women. Migraines occur with an estimated mean frequency of 1 to 2 per month. Headache severity is described as severe or very severe by 60% to 80% of migraine sufferers. Migraine has been stated by the World Health Organization to be one of the world’s most disabling medical illnesses.

In opposition to the great economic and quality of life impact due to the frequency and intensity of migraine headache, only about 56% of patients have ever had a medical diagnosis, and in the year 2000 only 17% had been given prescription drugs.²¹

People with migraine often have motion sickness either in childhood or adulthood. They usually cannot tolerate alcohol very well and many of them get a headache after drinking alcohol, especially wine or beer. Some persons with migraine get a headache at the end of a drink even though they don’t drink very much, only 1 or 2 glasses of wine. This factor alone is not enough to make a diagnosis but may be considered a marker for migraine.

The person with migraine has a sensitive brain and affected individuals may get attacks following exposure to bright sunlight, flashing lights or patterns, heat, nervous excitement, or fasting. In the first American Classification of Headache, migraine without aura used to be called common migraine because it is more prevalent, consisting of about 70% of all migraine attacks.²² Migraine has known sensitivities to light (photophobia), sound (phonophobia), and smell (osmophobia).

Typically, the patient has a one-sided headache (migraine comes from a Latin word that means half of head or hemicrania), nausea and vomiting, photophobia (fear of light), sonophobia (fear of sound), and goes to sleep in a quiet, dark room. This is often called a sick headache, sinus headache, heat or sun headache, menstrual headache, letdown headache (a headache that comes during a weekend, vacation, or holiday), cold-front or weather-change headache (from a drop in the barometric pressure), or nocturnal headache (middle-of-the-night, end-of-a-dream headache.) The patient may not know he has migraine but comes for treatment and diagnosis of a headache.

Migraine attacks may be precipitated by relaxation after stress—the weekend, holiday, or vacation headache. Headaches may come from oversleeping, anger, stress, freedom from stress, or from despair. The patients with migraine should consider that they have an overexcitable brain and that the attacks come from this over stimulation.

Michael Moskowitz, MD, at the Stroke Research Laboratory at Massachusetts General Hospital, Harvard Medical School, Boston, stated about the neurogenic inflammation, which involves vasodilation and plasma protein extravasation as a mechanism of headache pathogenesis.²³

The vasodilator peptides calcitonin gene-related peptides (CGRP), substance P, and neurokinins are found in the cell bodies of trigeminal neurons. CGRP levels increase during migraine.

Sterile neurogenic inflammation can occur in response to the vasoactive peptides substance P and neurokinins, which are released by the trigeminal vascular system. 5-HT 1D receptors have a prejunctional location at the neurovascular synapse between the trigeminal nerve and the dural vasculature.

Stephen Silberstein, MD, Director of the Jefferson Headache Center, in Philadelphia stated,²⁴

Headache probably results from activation of meningeal and blood vessel nociceptors (pain receptors). Trigeminal sensory neurons (neurons that innervate the orbits, jaws, and parts of the mouth) contain neuropeptides, such as substance P, calcitonin gene related peptide, (GGRP), and neurokinin A. Stimulation results in substance P and CGRP release from sensory neurons and from neurogenic inflammation. The afore-mentioned neuropeptides interact with the blood vessel wall, producing dilation, plasma protein extravasation (crossing through blood vessels into tissues) and platelet activation. Neurogenic inflammation sensitizes nerve fibers that now respond to previously innocent or harmless stimuli such as blood vessel pulsations causing, in part, the pain of migraine.

The triptans are a class of drug to treat migraine and there are 7 of them. They are all serotonin receptor specific agonists that abort migraine. There are also 5-HT 1D and B receptors located centrally at the trigeminal ganglion that, when activated, inhibit the conduction of pain signals from the site of the neurogenic inflammation and vasodilation in the meninges to the second order brainstem neurons mediating pain during migraine. 5-HT1D receptors located in the nucleus tractus solitarius of the brainstem inhibit central nausea and vomiting. All triptans activate both 5-HT1D and 5-HT1B receptors and all triptans have central and peripheral effects in humans.

Major comorbidities of migraine

Co means with, and morbidity refers to sickness or illness. To say that two conditions such as migraine and asthma are comorbid means that these conditions are observed to occur together more often than they would by chance.

Respiratory—allergic rhinitis and asthma (17%).

Cardiovascular—mitral valve prolapse, hypertension, angina, myocardial infarction.

Raynaud’s syndrome, stroke, hypertension or hypotension.

Endocrinological—thyroid disorders.

Gastrointestinal—ulcer disease, colitis, and irritable bowel syndrome (60%).

Rheumatologic—fibromyalgia (17%).

Neurologic—epilepsy, tension-type headache, and essential tremor.

Psychiatric—mood disorders, depression (50%), bipolar disorder.

Generalized anxiety disorder (34%), panic disorder, agoraphobia, chronic fatigue (20%), obsessive compulsive disorder.²⁵,²⁶,²⁷

The prevalence of epilepsy is 0.5% and of migraine is 12%. Six percent of patients with migraine have epilepsy and 8% to 15% of patients with epilepsy have migraine. A migraine aura may trigger a seizure (migralepsy) and a seizure may trigger a migraine attack.²⁸ An arteriovenous malformation of the occipital lobe and MELAS syndrome (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) are conditions that can trigger both migraine and epileptic attacks.²⁹ Severe prolonged migrainous symptoms and prolonged partial status epilepticus are characteristic features of the MELAS syndrome.

Temporal profile of a migraine attack

ICHD-3 states that migraine starts with premonitory symptoms.³⁰ The next thing to occur is the attack and then at the end comes recovery or post-migraine symptoms. Premonitory symptoms occur several hours to 1 or 2 days before the headache (migraine with or without aura) starts and the patient may have fatigue, trouble concentrating, neck stiffness, sensitivity to sound or light, nausea, blurred vision, yawning, pallor, an elated feeling, food cravings for sweet things to eat, feeling thirsty, drowsiness, irritability, or feeling depressed.

Some patients during these premonitory symptoms can’t define a specific symptom, yet they just know that soon they may get a headache. At this point there is no pain.

If the early symptoms are recognized as part of the migraine attack, the patient should treat during this time as this is the earliest sign, and the medication can start to work early and hopefully with great success.

During a typical attack, headache is the most noticeable symptom but nausea and then vomiting may occur hours later. Some patients report they feel better after they vomit. Then physical activity and sensitivity to light and sound become prominent and the patient retreats to her room where she may shut the door and turn off all the lights. Many victims go to sleep and when they awaken, they feel better.

However, the day after a poorly treated migraine, the patient may still have significant symptoms. There may be low level headache, listlessness, anorexia, and sensitivity to light, sound, and odors. The patient may have allodynia, which means that non-painful stimuli cause pain in the chemically stirred-up brain of the migraine patient.

Symptoms of allodynia would be pain from brushing one’s hair, where usually this is not a painful act. Allodynia may cause pain with wearing eyeglasses. Finally, after another day, the migraine patient is through with the suffering and back to a normal status.

One-sided headaches

The patient who was just interviewed described headaches that were behind one eye and felt like a white-hot poker or a needle; sometimes it throbs or feels like someone is trying to push my eyeball out. This is a common migraine pattern, linking to the idea that migraines are often (60% to70% of the time) one sided and in common arterial cranial sites—in the temple, behind one eye. Migraine comes from a mistranslation of the Latin word hemicrania, which comes down to the English-speaking world as migraine, a word that means half of head.

When I was a medical student and interested in neurology, my professor told me, Anytime you see a patient with pain behind one eye, it is migraine until proven otherwise. I have never forgotten that, and it helps me diagnostically every day.

Not all migraines have to be one sided, but many are. Some patients will relate that the headache will switch from side to side with individual attacks, which is a reassuring feature to the doctor who assumes the rotating retro-orbital (behind the eye) pain is migraine, a genetic generalized brain arterial problem, rather than something more concerning like an aneurysm, occurring always behind the same eye.

Pain in the neck

Migraines may also start in the neck and then move forward into the front of the head, settling behind one eye. Years back, most pain in the neck of non-traumatic origin was thought to be tension-type headache or arthritis, but the view on this has changed and the patient should be instructed to treat with their regular migraine medicine when the pain starts in the neck.

Activation of the trigeminal nucleus caudalis located in the brain stem is important in processing the pain of migraine. Pain signals brought to the trigeminal nucleus caudalis during migraine can also be relayed to central nervous system neurons in the thalamus and cortex.

The trigeminocervical network includes the 3 branches of the trigeminal nerve (ophthalmic, maxillary, and mandibular) that project to the face, as well as to sensory nerves in the back of the head and neck at C2 and C3.

Activation of the trigeminal nucleus caudalis may result in referred pain to various locations in the trigeminocervical network—forward into the face, behind one eye, in the temple or the cheek, or down into the medulla and upper cervical cord, causing pain in the neck and posterior occipital muscles, imitating what used to be called tension headache.

BRANCHES AND DISTRIBUTION OF THE NERVES OF THE FACE³¹

There are other factors of migraine pain that imitate tension-type headache. Although migraine may be one sided, RB Lipton, WF Stewart, S Diamond, et al., reported that 41% of migraine patients may at some time have bilateral pain.³²

J Olesen reported that 50% of the time, the pain of migraine was non-pulsating and 37% of patients with tension-type headaches may report pulsating pain.³³ These are important factors to consider when trying to make a headache diagnosis.

RG Kaniecki wrote in 2002 about assessing migraine and tension type headache. RG Kaniecki stated,³⁴

The difficulty in distinguishing episodic tension-type headache from migraine headache is widely acknowledged. The misdiagnosis of migraine as tension-type headache has potentially significant consequences because it may preclude patients with disabling headaches from receiving appropriate treatment. This article explores the symptomatologic, epidemiologic, and pathophysiologic relationships among migraine and tension-type headaches with the aim of elucidating ways to improve their diagnosis and treatment.

Clinical, epidemiologic, and pharmacologic data converge to suggest that rigid adherence to the IHS criteria in diagnosing migraine and tension-type headache may result in misdiagnosis of some headaches. Many migraine attacks are accompanied by tension headache-like symptoms, such as neck pain. Conversely, IHS-defined tension-type headaches are often accompanied by migraine-like symptoms, such as photophobia or phonophobia and aggravation by activity. The health-care provider caring for patients with headache should be cognizant of these overlaps and their implications for the management of patients with headache.

Throbbing headaches

The headache adjective and descriptive term throbbing implies a vascular etiology of the pain as blood courses through an artery with the beat of the heart, causing the artery to stretch and ache rhythmically.

A similar term would be pounding, or the patient may say like a hammer. This rhythmic vascular pain relates to vasodilation and chemical inflammation of cerebral arteries. For years, vasodilation was thought to be the main cause of the pain of migraine, but later views have considered pain arising also from a sensitized trigeminal nerve.

Frequency of headache

Determining the frequency of migraine is important for making the diagnosis for deciding treatment and gauging disability. Migraine is defined as a periodic headache, that is, a period of time of headache surrounded by a period of time without headache.

Tension-type headache often occurs every day, albeit at different levels of intensity. Someone who has dull, daily, mild-to-moderate headaches every day for months oftentimes has a diagnosis of tension-type headache.

Patients who earlier in life had a history of regular migraine but who later develop severe pounding, life limiting headaches every 2 to 3 days that get better only temporarily with frequent headache medication is likely someone with migraine who is overtreating themselves with medication and has developed the syndrome of medication-overuse headache. This is a very common pattern different from regular migraine in that the patient often doesn’t have long headache-free times between headaches.

If the patient is experiencing more than 2 to 4 migraines a month, the physician might consider offering preventive medication to be taken daily to reduce the total number of migraines.

Severity of headache

The degree of severity of the headaches helps make the diagnosis. Migraines tend to be at least moderate, but usually severe headaches. Tension-type headaches tend to be mild to moderate. On a numerical scale of 1 to 10 where 10 is more severe, migraine patients usually say 10 plus or 20 while tension-type headaches are described as 1 to 5.

The severity factor impacts the patient’s level of activity. Patients with tension-type headache usually can stay in their lives, continue to work, and stay up till bedtime, whereas migraine patients cannot.

Duration of headache

ICHD-3 states that migraine without aura may last 4 to 72 hours and this time interval might be expressed as half a day or 3 days.³⁵ Most patients would say their migraines last half a day, all day, or rarely several days.

But the point would be that the pain would have a beginning and an end. It would be a periodic headache, surrounded by a time in life with no headache. Patients who describe migraine headaches as lasting a week or a month or continually are describing medication-overuse headache.

Menstrual headache

ICHD-3 defines menstrually related migraine without aura as occurring between days -2 and +3 in at least 2 out of 3 menstrual cycles.³⁶ The first day of menstruation is day 1 and the preceding day is -1; there is no day 0. It is estimated that 60% of female migraineurs have menstrual migraine without aura.

Many women would say, especially during their younger years of menstruation and before they are anywhere near menopause, that they have fairly regular cycles, often predictable to the day. Other women are not so orderly on the date the cycle comes and may be off a day or several days, or they may not even have a menstrual cycle every month.

These menstrual migraines are often the worst and most disabling headache the migraine patient may suffer each month. They will say the pain is more intense, and the associated symptoms of nausea and vomiting, and sonic and photic sensitivity are worse.

They are more likely to be confined to their bed with this particular migraine and may miss work or be out of their lives.

Menstrual attacks are chiefly migraine-without-aura-type headache. Women who have both migraine with and without aura usually only have migraine-without-aura attacks with menstruation. One theory regarding menstrual attacks is that they result from estrogen withdrawal.

TYPICAL MONTHLY HORMONAL LEVELS³⁷

Menstrual migraine without aura flares during times of hormonal fluctuations during the reproductive years but is less active during times of hormonal stability, such as before menarche or after menopause. As a woman goes through life’s stages, her hormonal status has a great effect on migraine.

Menstruation, pregnancy, the use of oral contraceptives, menopause, and hormone therapy influence the incidence and management of migraine.

BS Tozer, EA Boatwright, PS David, et al., writing in the Mayo Clinic Proceedings in 2006 on Prevention of migraine in women throughout the life span, stated, Fluctuating hormone levels may exacerbate migraine during perimenopause, making the menopausal transition particularly challenging for female migraineurs.³⁸

ICHD-3 recognizes that some women only have menstrually related headache but no migraine at other times during their cycle. This is called pure menstrual migraine without aura and comprises 14% of women with migraine.³⁹,⁴⁰ Women who have attacks at menstruation and at other times during the cycle are called menstrually related migraine without aura.⁴¹

The importance of the pure menstrual migraine group is that some studies show that hormone prophylaxis may be more effective for this type of migraine.

A lay myth is that migraine goes away at menopause. Long-term studies do not support this myth. CWM Whitty and JM Hockaday reported on what happens to patients with migraine in their article in the British Medical Journal in 1968 titled, Migraine: a follow-up study of 92 patients.⁴²

They start their article with the following comments:

It has been a commonly held view that migraine attacks tend to cease as time passes and that such improvement occurs particularly after the menopause in women. However, we have found no published work on the natural history of the condition over periods of more than a few years which might lend support to this view.

We therefore studied a group of migraine patients followed for periods of 15 to 20 years who, when finally assessed, had been subject to the condition for 16 to 69 years. We inquired for changes in frequency and severity of attacks and in the pattern of individual attacks and sought to find out if these showed any consistent relation to advancing years, to the menopause, or to intercurrent illness, especially the development of hypertension or cervical spondylosis.

In conclusion, CWM Whitty and J Hockaday stated,

We found no evidence to support a commonly held view that migraine improves or ceases with the menopause. Most of our cases showed no change; rather more were worse than better. One patient started her attacks, which we believed to be true migraine by the usual criteria, at the menopause.

These same women may have an increase in frequency, intensity, and type of migraine attacks with the use of birth control pills or estrogen.⁴³

Other women with migraine may notice no particular relationship to their menses or estrogen levels. This is likely due to different genes for migraine.

In October 2006, the National Menstrual Migraine Coalition (NMMC) was formed to address the need for greater awareness of menstrual migraine.⁴⁴ The NMMC consists of organizations and clinicians in the fields of neurology, primary care, obstetrics and gynecology, managed health care, and women’s health.

Migraine and pregnancy

Although migraine is less active for many women during pregnancy when hormonal levels are high and more stable, migraine may begin for the first time during pregnancy, especially in the first trimester.

Many women with menstrually related migraine without aura or migraine with aura have little headache during pregnancy, only to have the attacks return with resumption of the menstrual cycle.⁴⁵ During pregnancy usually migraine with aura is seen.⁴⁶

A Uknis and SD Silberstein writing in Headache in 1991 on Migraine and pregnancy presented a case⁴⁷:

A 27-year-old woman with no family or personal history of migraine presented with headache associated with unilateral paresthesias and blurred vision.

This was her first, and so far, only, attack of migraine with aura and led to the diagnosis of her pregnancy and to this review.

A Uknis and SD Silberstein also stated,

Preexisting migraine usually improves with pregnancy, particularly if it was associated with menstrual migraine.