Do you know the difference between migraine as a headache and migraine as a disease? - Learn about the "Migraine Brain"
"A CORRECT DIAGNOSIS IS THREE-FOURTHS THE REMEDY." - M. K. Gandhi
MIGRAINE AS A HEADACHE
Almost everybody gets a headache sometime in their lives. Because so many people suffer from headaches and headaches have numerous causes, many of which can be life-threatening, the International Headache Society developed a classification system to help doctors provide accurate diagnoses and offer effective treatments for their patients. As well, the specific diagnostic criteria must be fulfilled for patients to be entered into research projects.
The most recent edition of The International Classification of Headache Disorders (ICHD) is the -3 beta version (ICHD-3 beta). The document is extensive. To address its entirety is beyond the scope of this article. Therefore, to give us an idea of the numerous types of headaches a person might experience, we take a brief glimpse at the ICHD-3 beta list of Classifications and Diagnosis (for a more complete list, see Cephalalgia, pages 636-685). In this version, headaches are classified as:
1. Primary: (are caused by independent pathomechanisms)
- Migraine: including migraine without aura, migraine with aura (aura with headache and aura without headache; migraine with brainstem aura; hemiplegic migraine and types of familial hemiplegic migraine; sporadic hemiplegic migraine; and, retinal migraine), chronic migraine, complications of migraine (Status migrainous, Persistant aura without infarction, Migrainous infarction, Migraine aura-triggered seizure), probable migraine, and episodic syndromes that may be associated with migraine like cyclical vomiting syndrome and abdominal migraine
- Tension-type headache: including infrequent episodic, frequent episodic, chronic, and probable
- Trigeminal autonomic cephalalgias (TACs): including cluster headache, paroxysmal hemicrania, hemicrania continua
- Other primary headache disorders: including primary cough headache, primary exercise headache, primary thunderclap headache, primary stabbing headache, and new daily persistent headache (NDPH)
2. Secondary: (a secondary symptom to another disorder known to cause headache)
- Headache attributed to trauma or injury to the head and/or neck: including head trauma, whiplash, and craniotomy
- Headache attributed to cranial or cervical vascular disorder: including ischemic stroke or transient ischemic attack (TIA), intracranial hemorrhage, giant cell arteritis GCA)
- Headache attributed to non-vascular intracranial disorder: including increased cerebral spinal fluid pressure, idiopathic intracranial hypertension (IIH), low cerebral spinal fluid pressure, intracranial neoplasm, epileptic seizure
- Headache attributed to substance or its withdrawal: including carbon monoxide-induced headache, alcohol-induced headache, headache by food or additive (monosodium glutamate-induced headache), cocaine-induced headache, histamine-induced headache, calcitonin gene-related peptide-induced headache, medication-overuse headache (MOH)
- Headache attributed to infection
- Headache attributed to disorder of homeostasis: including hypoxia and/or hypercapnia, high altitude headache, airplane travel, driving, sleep apnea, dialysis, pre-eclampsia or eclampsia, hypothyroidism, fasting
- Headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cervical structure: including cervicogenic, glaucoma, acute and chronic rhinosinusitis, temporomandibular disorder (TMD)
- Headache attributed to psychiatric disorder
3. Painful cranial neuropathies, other facial pains and other headaches: including trigeminal neuralgia, occipital neuralgia, optic neuritis.
Keeping these things in mind, it is important for us to know that a person may receive more than one primary headache diagnosis. For example, in my case I have migraine with aura, migraine without aura, and tension-type headache. As well, we may have a primary headache and receive a diagnosis for a secondary headache such as medication overuse headache or cervicogenic headache.
Another point to be aware of is that headache is a phase of a migraine attack. A migraine attack is considered to have four phases: premonitory (prodrome), aura, headache, and postdrome (resolution). Not all of us go through each phase. For instance, you may never have an aura. Another person may have an aura without a headache (see ICHD-3 beta, pages 645-650 for specific diagnostic criteria).
In addition, we need to know migraine attacks may be episodic or chronic. Episodic migraine (EM) includes a range of attack frequency with headache days 0-14 days per month. If our headache days occur on 15 or more days per month (tension-type or migraine-like) for more than 3 months, with the features of migraine headache on at least 8 days per month, we are given the diagnosis chronic migraine (CM). We should know that the most common cause of symptoms of chronic migraine is medication overuse (ICHD-3 beta).
This brings us to a discussion about migraine as a disease.
"AWARENESS IS THE GREATEST AGENT FOR CHANGE". - Eckhart Tolle
MIGRAINE AS A DISEASE
Migraine is believed to be a genetic neurological disease. As persons with migraine, we are thought to have an inherited sensitivity of the nervous system that makes our brains (neurons) hyperexcitable. This hyperexcitability gives us a predisposition to migraine attacks. Although research continues to explore the exact cause of migraine, a number of areas in our brains are thought to be directly or indirectly involved in the complex pathogenesis, including the hypothalamus, brainstem, cortex, limbic system, and the trigeminovascular pathway (Charles, 2012; Burstein et al., 2015; Maniyar et al., 2015).
That said, in the Burstein article, during a discussion of disease mechanisms, the authors report, "migraine attacks are likely to begin centrally, in brain areas capable of generating the classical neurological symptoms of prodromes and aura, whereas the headache phase begins with consequential activation of meningeal receptors at the origin of the trigeminovascular system" (p. 6620). Here, it is important for us to know that as a migraine attack progresses through these phases, a number of electrical and chemical events take place, including the involvement of neurotransmitters, neuropeptides, and proinflammatory mediators such as dopamine, serotonin, norepinephrine, glutamate, nitric oxide, calcitonin gene-related peptide, histamine, bradykinin and protaglandins. The entire range of these mechanisms is thought to be associated with the wide variety of symptoms we experience (Charles, 2012; Burstein, et al., 2015; Maniyar et al., 2015).
Let's take a brief look at some examples (for more detailed discussions, see references cited):
Premonitory (prodrome) phase:
Premonitory symptoms may precede the headache phase of a migraine attack, with or without aura. A number of symptoms have been reported, including fatigue, euphoria, depression, irritability, food cravings, constipation, neck stiffness (pain), yawning, difficulties with concentration, nausea, blurred vision, bloating, pallor, change in facial expression or body perception, piloerection, and sensitivity to light, sound, and smell (Charles, 2012; ICHD-3 beta, 2013; Burstein, et al., 2015; Maniyar, et al., 2015). In the Burstein article, the authors report premonitory symptoms most commonly described by patients point to the potential involvement of:
- the hypothalamus, including symptoms fatigue, depression, irritability food cravings, and yawning;
- the brainstem, including symptoms muscle tenderness and neck stiffness;
- the cortex, including symptoms abnormal sensitivity to light, sound, and smell; and
- the limbic system, including depression and anhedonia (p. 6620).
In addition, both the Charles and Maniyar articles suggest premonitory symptoms may be associated with the hypothalamus and note the neurotransmitter dopamine may play an important role. In the Maniyar article, the authors also report emotional changes and a feeling of tiredness may result from involvement of limbic/frontal areas mediated by the hypothalamus; posterior hypothalamic dysfunction could explain neck discomfort and stiffness; and, involvement of the frontal cortex could explain difficulties in reading, writing, and concentration (p. 611). It is interesting to note that in the Charles article, the author mentions some premonitory symptoms may come and go before the headache phase, others may build up in intensity leading up to the headache, occur during the headache, and persist well beyond the resolution phase (p.413).
Aura may begin before pain, after headache has started, or continue into the headache phase. (ICHD-3 beta, 2013; Maniyar, et al., 2015). In the Burnstein article, the authors report aura symptoms point to the potential involvement of:
- the visual cortex, including scintillating lights* and scotomas*;
- the somatosensory cortex, including paresthesia, and numbness of the face and hands;
- the motor cortex or basal ganglia, including tremor and unilateral muscle weakness; and
- the speech area, including difficulty saying words or aphasia (p. 6619).
*Scintillating lights are visual hallucinations that are bright and fluctuate in intensity. Scotoma is defined as loss of part(s) of the visual field of one or both eyes (ICHD-3 beta, 2013, p. 808).
Headache is usually unilateral, pulsating, moderate to severe intensity, and may be aggravated by movement but may be felt all over the head, (on one or both sides and in the middle of the head), including the eyes, frontal, occipital and neck areas (Kelman, 2005; ICHD-3 beta, 2013; Burstein, et al., 2015). In the Burstein article, the authors report, as headache progresses, we may experience a variety of:
- autonomic symptoms, including nausea, vomiting, nasal/sinus congestion, rhinorrhea (runny nose), lacrimation (tearing one or both eyes), ptosis, drooping of upper eyelid) yawning, frequent urination and diarrhea:
- affective symptoms, including depression and irritability;
- cognitive symptoms, including attention deficit, difficulty finding words, transient amnesia, reduced ability to navigate in familiar environments; and,
- sensory symptoms, including photophobia (sensitivity to light), phonophobia (sensitivity to sound), osmophobia (sensitivity to smell), cutaneous allodynia (sensitivity to touch) and muscle tenderness (pages 6619-6620).
POSTDROME (RESOLUTION) PHASE
Some symptoms may persist beyond the headache phase. Postdromal symptoms are thought to be similar to those in the premonitory phase and may include:
- hyperactivity or hypoactivity (tiredness, weakness, fatigue);
- cognitive difficulties;
- mood change (depression);
- residual head pain, lightheadedness;
- neck pain and/or stiffness;
- food cravings; and,
- gastrointestinal symptoms (Charles, 2013; ICHD-3 beta, 2013).
"WITHOUT KNOWLEDGE ACTION IS USELESS AND KNOWLEDGE WITHOUT ACTION IS FUTILE." - Abu Bakr
Numerous sources commonly refer to migraine as a severe headache. However, as the authors of the Burstein article report, the extent of our symptoms suggests that "migraine is more than a headache. It is now viewed as a complex neurological disorder... and as such, it is evident that the migraine brain differs from the nonmigraine brain" (p. 6620).
The authors also mention that "because the migraine brain is extremely sensitive to deviations from homeostasis (wake-sleep cycles, body temperature, food intake, etc.), it seems reasonable that hypothalamic neurons that regulate homeostasis and circadian cycles are at the origin of some of the migraine prodomes" (p. 6629). In line with this, the Maniyar article indicates hypothalamic involvement can explain many of the premonitory symptoms. Here, the authors suggest further research is needed to investigate whether treatment during the premonitory phase can reliably prevent headache in patients who are able to predict the headache phase of a migraine attack (p. 618).
And, lastly, we should know the Charles article reports "a comprehensive approach of migraine demands appreciation of all the phases of an attack and the development of future therapies may hinge not only on an understanding of what goes on in the brain during a headache but also what happens in the hours before it begins and after it ends" (p. 417).
Burstein, R., Noseda, R., & Borsook, (2015). "Migraine: Multiple Processes, Complex Pathophysiology". The Journal of Neuroscience. April;35(17): 6619-6629.
Charles, A. (2013). "The evolution of a migraine attack - a review of the evidence." Headache. Feb;53(2):413-9.
Headache Classification Subcommittee of the International Headache Society. The International Headache Society. "The International Classification of Headache Disorders: 3rd edition (beta version). Cephalalgia. 2013;33:629-608.
Kelman, L. (2005). "Migraine pain location: a tertiary care study of 1283 migraineurs." Headache. Sep;45(8):1038-47.
Maniyar, F. H., Sprenger, T., Monteith, T., et al., (2015). "The premonitory phase of migraine-what can we learn from it?" Headache. May;55(5) 609-20.
Sharron Murray M.S., R.N. is the author of Migraine: Identify Your Triggers, Break Your dependence On Medication, Take Back Your Life. San Francisco:Conari Press, 2013.
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 October 9th, 2016
Copyright June 1st, Sharron E Murray, 2016