Migraine, headache, and facial pain tips

Migraine, headache, and facial pain tips provides general information, education, and tips on many topics for a wide variety of headache, migraine, and facial pain disorders.

Last updated on October 22nd, 2020 at 12:09 am




Covid-19 headache, coronavirus headache, Covid headache and Covid19 headache are all terms for the same headaches which have been on the rise thanks to Coronavirus (Covid-19). This has been happening in patients who have gotten infected with Covid-19. We’ll be discussing that in much greater detail further down, as well as how to treat Covid-19 headache. Interestingly though, migraines and headache have been worsening in patients who have not been infected at all as well. So how is Covid-19 worsening headaches in patients who haven’t been infected? This phenomenon on worsening headaches related to Covid-19 in patients who haven’t been infected is predominantly occurring in patients with migraine. Let me tell you the reasons why.


Why are my migraines worse since Covid-19 and how are they treated?

We look at migraine as an electrical neurological event. It is no longer considered a “vascular headache”, which older terminology suggested. People with migraine have a hypersensitive, or hyperactive, neurological system. So when they encounter triggers, their migraine circuitry switch turns on easier, compared to someone without a migraine history. Basically, they have a lower threshold to trigger a migraine compared to someone without migraine.

Stress is a major, major migraine trigger, and one of the top triggers. Did I mention it is a MAJOR migraine trigger? Ok, you get the point. In addition to stress, there are a wide spectrum of triggers ranging from weather changes, hormones, foods, food additives, too little sleep, excess sleep, and a whole array of others. However, let’s talk about Covid-19 stress.

Unless you’ve been living in isolation in a doom’s day bunker deep in the remote countryside, the Covid-19 pandemic has been very stressful on everyone. So not surprisingly, migraine has also been much worse in general for patients with migraine given these increased stress levels. Everyone’s world has been turned upside down with Covid-19. Our routines and life as we’ve known it were abruptly changed. Parents suddenly became teachers at home, despite no knowledge or ability of knowing how to teach. Screen time skyrocketed (which is often a migraine trigger) from virtual teaching, virtual school, Zoom meetings, and a whole spectrum of other nightmarish virtual work meetings. The frequent crashing of these virtual platforms for many people is also very stress inducing, and likely led to some broken computer screens followed by unanticipated repair costs, and ok, you get the point here. People became socially isolated, which worsened mood for many people, and this often correlates with migraines worsening as well. Spouses and family members found themselves in quarantines and spending way more time together than they were used to or liked to, and that can also be stress inducing for many couples. Kids were home constantly, needing entertainment for their perpetual “I’m bored” complaints, basically just never letting parents get a break, and there were many reports of children actually turning into demons at home. Ok, maybe not, but I think you get the picture. The bottom line is that there have been many changes in our normal routines which were often very intrusive, disruptive, and stress inducing.

Treatment of the increased migraine frequency during Covid-19 (or any other time of increase) consists of typical management strategies. Conservative measures including well techniques, yoga, medication, diet, hydration, proper sleep and exercise certainly play a role. If frequency remains high, then preventive treatment should be considered for a few months until migraines improve. Having 4 or more migraines per month is a general guideline of when a preventive treatment is often considered. Preventive treatments include natural therapies, supplements and nutraceuticals, daily medications, CGRP monoclonal antibody therapy, and neuromodulatory devices.


What is Coronavirus (Covid-19) Headache?

First of all, the International Classification of Headache Disorders 3rd Edition (ICHD-3) accounts for Headache attributed to systemic viral infection, which is common with many nonspecific infections including viral infections such as the common cold or other upper respiratory viral infections. So headache is certainly not specific only to Coronavirus, but it is common with many common viral infections. These types of nonspecific headaches are diagnosed with the following criteria:


  1. Headache of any duration fulfilling criterion C
  2. Both of the following:
    1. systemic viral infection has been diagnosed
    2. no evidence of meningitic or encephalitic involvement
  3. Evidence of causation demonstrated by at least two of the following:
    1. headache has developed in temporal relation to onset of the systemic viral infection
    2. headache has significantly worsened in parallel with worsening of the systemic viral infection
    3. headache has significantly improved or resolved in parallel with improvement in or resolution of the systemic viral infection
    4. headache has either or both of the following characteristics: a) diffuse pain, b) moderate or severe intensity

4. Not better accounted for by another ICHD-3 diagnosis


Coronavirus (Covid-19) headache refers to headaches that have been triggered in direct relation to becoming infected with Covid-19, which is also associated with a variety of other symptoms and a positive Covid-19 test. First of all, if you already have migraine, you will generally be much more likely to have an increase in headaches since your internal electrical wiring already predisposes you to having headaches easier when the body is under any stress (emotional, physical, infection, stress, etc.), as discussed above. So if you get infected with Covid-19, you may have an increase in your baseline migraines for this reason, similar to what often happens with other types of infections (including the common cold). However, headache is a common (and often early) Covid-19 symptom in patients who do not have a migraine or headache either, similar to headaches which can be caused by many other types of infections as well.

The Covid-19 associated headache is often daily and commonly has migraine characteristics (throbbing, pounding, nausea, sensitivity to light and sound), or it can have tension type headache character (dull achy pressure throughout head), or a combination of both. One small study reported that Covid-19 associated headaches also had some unusual features, including new rapid onset unrelenting pain (including a thunderclap headache presentation), higher intensity, and association with anosmia/ageusia (loss of smell/taste), diarrhea, reduced appetite, and weight loss.

Coronavirus headache may also present with a story which fits well with New Daily Persistent Headache (NDPH). This is a headache that begins as a daily headache and persists as daily for more than 3 months, without any other known cause. Classically, patients with NDPH often will come into the office and tell you the specific date the headache began and that it has never gone away since. It may fluctuate in the severity levels, but it never fully goes away. It often has an overlapping mixture of migraine characteristics (throbbing, pounding, nausea, sensitivity to light and sound), and tension type headache characteristics (dull achy pressure throughout head). NDPH most often occurs without a clear reason. However, notably one of the most common associations if there is one is a nonspecific viral infection such as a cold or upper respiratory infection that precedes the headache. Covid-19 is simply another type of virus which can be associated with this form of headache.


How is Coronavirus (Covid-19) Headache treated?

Treatment of Covid-19 itself should follow current guidelines as directed by your regular doctor as well as the CDC (Centers for Disease Control) and WHO (World Health Organization) guidelines. Beyond this, treatment of Coronavirus headache revolves around symptomatic treatment. This basically means you are treating the symptoms rather than the virus itself, as is the case with the majority of viral infections (such as common cold viruses) besides treatable ones such as herpes simplex virus (HSV) and varicella zoster virus (VZV). If the headaches have migrainous features, they can be treated as migraine, tension-type headache, or NDPH with acute/abortive options, and preventive daily treatment options if the frequency of headaches remains high and is not improving.



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Last updated on October 20th, 2020 at 06:41 am





I see patients in our headache center from all over the United States and from many other countries. Many patients travel hundreds of miles by car or airplane for these visits, due to the shortage of available headache specialists (about 570 in the US). Many patients are lucky enough to be relatively close to a headache specialist. Whichever scenario you fall into, you want to get the most out of your appointment with a headache specialist in order to get on a better path to less headache or facial pain burden.


When to see a headache specialist

So first of all, when should you see a headache specialist? First off, any type of headache, head pain, or facial pain, is reason enough to see a headache specialist. Basically, headache specialists specialize in any type of pain or discomfort involving anywhere in the head or face. They also commonly see patients that may have other neurological symptoms which may not necessarily be associated with headaches, but their doctor wants to rule out a migraine “equivalent” disorder. Some patients can have neurologic symptoms without headache (visual, sensory, speech, vertigo, weakness, nausea/vomiting, abdominal pain), which may actually reflect a painless migraine disorder, such as migraine aura without headache. I have compiled a list below of a few of my thoughts of when your headache or facial pain treatment journey signals that it is time to see a headache specialist.


Reasons to see a headache specialist:

-You have a headache, head pain, or facial pain.

-Your doctor tells you, “your headache is all in your head”.

-Your doctor tells you, “there’s nothing else I can do for you”.

-Your doctor says, “I don’t treat much headache, but…”.

-You continue to have frequent headaches despite trying several preventive medications.

-You just don’t feel like you are making any progress despite a couple office visits with your doctor or their NP or PA (or you never even get to see the doctor).

-You don’t feel like your doctor is listening to you or taking your symptoms seriously.

-The doctor spends only a few minutes in the visit, so you feel rushed and unable to discuss all of your concerns.

-Your doctor is googling your symptoms in the office.

-Your doctor recommends that you take opiates/opioids for migraine treatment.

-Your doctor says it is ok to use NSAIDs, OTCs or triptans more than 10 days per month or butalbital/fioricet/fiorinal more than 5 days per month on average for migraine treatment.

-Your doctor says your headache is “because you are depressed”.

-Your doctor does not give you a more specific classification or name for your diagnosis.


What information should you gather before the visit?

Unfortunately, we all know how strapped for time most physicians are during office visits due to a variety of factors such as low insurance reimbursement and the need to increase patient volume to compensate for this and break even. So to get the most out of your office visit, making it efficient and helpful, it is important to compile certain information in preparation. Typing out this information and bringing it to your office visit is a great idea. It is also a great idea to keep this as a running file that you can continue adding to in your personal files. This helps to eliminate time wasted in the office that could easily be organized and thought through prior to the visit, allowing more time for the important parts of the office visit; optimizing the diagnosis and treatment plans. Some of this information you may not have available, and that is certainly ok. You may be able to retrieve some of it from records, memory, and your local pharmacist.

Never assume that your local doctor’s office has faxed all of your records ahead of the visit. If that happens, great. However, many times patients are told that the records will be sent, but when we see the patient, we have no records that were sent. So, it is always best to bring all of your records yourself. Furthermore, it is good to have copies of all of your medical records, testing, etc. for your personal files anyway.


The following list are items that I have found to be the most useful for patients to have gathered and thought of prior to the visit, allowing the most efficient and useful office visit:

A) Acute/abortive headache or pain treatments (used “as needed”). This information is also needed in order to pursue insurance approvals for various types of treatments such as the newer gepants (Ubrelvy, Nurtec) or ditans (Reyvow).

-All that have been tried (which triptans, NSAIDs, neuromodulation devices, etc.)

-Doses used

-Responses (effectiveness, side effects) of each treatment


B) Preventive headache or pain treatments (used daily to lessen headache frequency/severity). This information is also needed in order to pursue insurance approvals for various treatments such as Botox or the CGRP mAb antagonists (Aimovig, Ajovy, Emgality, Vyepti).

-All that have been tried

-Maximum doses used

-Duration that each treatment was used

-Responses (effectiveness, side effects) of each treatment


C) Testing

-All CD and radiology reports for all brain MRIs, CTs, and other relevant testing for your headache or pain. Most CDs do not include the radiology report, and you need to request that separately. It is a good idea to have copies of all of these things for your personal files regardless. Bring them all to the office visit for the doctor to review.

-All bloodwork done in the past 5 years. Labs particularly important for headache evaluations include TSH, CBC, CMP, Vitamin D, Vitamin B12, ESR, CRP, ANA, to name a few, but this may vary and include more or less, depending on the specific clinical scenario.


D) Think about the clinical features of your headache or facial pain as listed below. These will be important questions that your headache specialist will ask. So, it is good to answer these questions in your head prior to the visit, so you can provide more accurate and thought out answers. This helps to prevent being put on the spot by questions you never really thought about which may result in forgetting some important details. For a free headache and facial pain self-diagnosis tool which incorporates all of these important questions that a headache specialist asks, look here.

-Location of the headache or facial pain

-Frequency of the headache or facial pain attacks

-Duration of the headache or facial pain attacks

-Description and characterization of the headache or facial pain attacks

-Neurological symptoms associated with the headache or facial pain (visual disturbances, numbness, tingling, weakness, speech disturbances, vertigo, etc.)

-Other associated symptoms with the headache or facial pain (nausea, sensitivity to light or sound, one sided autonomic features (runny eye, red eye, runny or congested nose, droopy or puffiness around eye))



If you are able to gather all or much of the above listed information prior to your headache specialist appointment, you’ll be well on your way to a much more efficient and beneficial office visit. As a result, you and your doctor will be able spend more time in the office discussing the most important things rather than spending it trying to look up records or digging through your memory for various details. As a result, your doctor will have more time to better formulate a list of the most likely diagnoses, and best treatment approaches for minimizing the disruption of your headache or facial pain on your life. Good luck!!





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Last updated on October 20th, 2020 at 05:19 pm




The International Classification of Headache Disorders-3 (ICHD-3) classifies persistent aura without infarction (stroke) and migrainous infarction as two of the four reported complications of migraine, both of which are very rare. The other two reported complications of migraine include status migrainosus and migraine aura-triggered seizure, but these will not be discussed here1. 



In order to discuss persistent migraine aura without infarction or migrainous infarction, it is crucial to understand migraine pathophysiology, which involves a multitude of complex processes throughout the cortex, brainstem, and cerebral vasculature. The pathophysiology of migraine has evolved from the vascular theory to the neurovascular theory of migraine. The older vascular theory proposed by Wolff viewed migraine as beginning with cerebral vasospasm causing focal ischemic (lack of blood flow) symptoms (aura) followed by extra and/or intracranial hyperperfusion (excess blood flow) from vasodilatation leading to the migraine pain. 2 This theory made good sense for how stroke or persistent neurological symptoms could develop, from the period of cerebral vasospasm and constriction. However, in later studies of migraine with aura, regional hypoperfusion developed before and outlasted focal neurologic symptoms, and this dissociation of time, perfusion changes and symptoms indicated that these neurologic symptoms were not caused by truly ischemic blood flow, but rather the apparent hypoperfusion is secondary to a disturbance in brain metabolism. 3-6

Lashley first described his own visual aura and hypothesized that the aura was due to a spreading abnormality migrating over the visual cortex at a rate of 3-5 mm per minute in 1941. 7 In 1944, Leão described spreading depression as a wave beginning with a brief neuronal burst associated with transient increased blood flow followed by a longer lasting neuronal electrical suppression with decreased blood flow in an animal model. 8-10 Subsequent studies confirmed this initial focal hyperemia followed by posteriorly to anteriorly spreading oligaemia (reduced blood flow) and regional cerebral blood flow reduction, which does not reach critical ischemic values, in a wave-like manner at approximately 2-5 mm per minute. This spreading regional cerebral blood flow reduction is independent of arterial territories, and does not cross cytoarchitectural borders or neuronal discontinuity such as the central sulcus or lateral sulcus, confirming impaired neuronal metabolism with subsequent regional cerebral blood flow reduction, rather than true ischemia. 3-6 This remains the basis for the now current neurovascular theory of migraine.

Most studies have been unable to show significant ischemic cerebral blood flow changes during migraine attacks. Results have shown alterations in cerebral blood volume, relative cerebral blood flow, and tissue mean transit time (MTT) in the grey matter of the occipital cortex contralateral (opposite) to the side of aura during an attack, while others have shown global cerebral blood flow increase, and others have shown hypoperfusion of the whole hemisphere, but never true ischemic hypoperfusion. 11-14 Notably, cerebral blood flow changes correlate poorly with migraine pain, and neurogenic inflammation in the trigemino-vascular system is suspected to be the primary cause of migraine pain, rather than arterial vasodilatation. 11,15



The ICHD-3 defines persistent aura without infarction as aura symptoms persisting for 1 week or more without evidence of infarction on neuroimaging. It should occur in a patient with a history of migraine with aura and typical of previous auras except that one or more aura symptoms persist for 1 week or more. Neuroimaging must show no evidence of infarction, and symptoms are not better accounted for by another ICHD-3 diagnosis. The aura symptoms are often bilateral and may last for months or years. It is important to differentiate persistent aura without infarction from symptomatic aura as a result of cerebral migrainous infarction. Aura symptoms lasting more than 1 hour and less than 1 week are classified as probable migraine with aura.

There are two primary types of persistent migraine aura that are described. One is persistent primary visual disturbance in which the patients describe “visual snow” or “television static” in both visual fields in both eyes, and some report additional intermittent scotoma or oscillating lights. 16 The other is persistent migraine aura with typical aura, in which patients describe scotoma, fortification, or oscillation in one hemifield (one side of vision), and does not go away (sometimes also called status aura). 16

The specific pathophysiology of persistent migraine aura without infarction remains unknown, although several theories exist. Some of these theories include low cerebral magnesium levels, abnormal cerebral energy metabolism, greater cerebral reactivity of NMDA receptors to glutamate, lower threshold for triggering cortical spreading depression, low cortical preactivation due to thalamocortical hypoactivity, sustained hyperexcitability of the visual cortex without significant dynamic modulation, sustained cortical neuronal dysfunction, intracortical disinhibition, loss of inhibitory GABA-ergic interneurons resulting in a network imbalance leading to a reverberating cycle of cortical spreading depression (small cortical infarctions below MRI sensitivity in the occipital cortex has been one proposed mechanism), or a combination of any of these possibilities. 16-21

The evaluation for persistent migraine aura without infarction should focus on excluding intracranial pathology, primarily stroke, although other intracranial etiologies need to be excluded. Brain MRI scan is preferable with MRA of the brain and neck (to also assess the arteries), but if medically contraindicated, brain CT scan with CTA of the brain and neck (to assess the arteries) can be pursued. Contrast administration for either type of scan is suggested, although not mandatory. A detailed neuro-ophthalmologic examination is also required. Studies investigating other imaging modalities for persistent migraine aura without infarction, including FDG-PET, MR-PWI, and Tc99m-HMPAO-SPECT, have shown conflicting and inconsistent results.

Treatment for persistent aura without infarction is undefined, and generally based on medication trial and error. The literature reveals an extensive list of medications tried and failed, with most attempting to target neuronal hyperexcitability. Treatments and medications which have been assessed have included anticonvulsants (lamotrigine, topiramate, valproic acid, gabapentin, phenobarbital, phenytoin, carbamazepine), benzodiazepines (clonazepam, diazepam), antidepressants (amitriptyline, cymbalta, buspirone, fluoxetine, nortriptyline, sertraline, dothiepin), anti-hypertensive (atenolol, acetazolamide, flunarazine, metoprolol, propranolol, verapamil, nifedipine, nimodipine, furosemide), NSAIDs (acetylsalicylic acid, ibuprofen, flurbiprofen, diclofenac, indomethacin, naproxen) analgesics (acetaminophen, butalbital, codeine), and a variety of other medications (baclofen, citicholine, ergotamine, ketamine, cyproheptadine, methylphenidate, methylprednisolone, pizotifen, prochlorperazine, promethazine, sumatriptan, memantine). The vast majority of these medications have shown no evidence of benefit. 16 Of them, lamotrigine has shown the most evidence of benefit, while divalproex sodium, baclofen, sertraline, nifedipine, nimodipine, acetylsalicylic acid, and furosemide have reported varying degrees of benefit from complete to partial resolution of symptoms. 16   

Abortive migraine options can include the gepants (Ubrelvy, Nurtec ODT), ditans (Reyvow), NSAIDs and other conventional abortives, although triptans and ergots should be avoided.



The ICHD-3 defines migrainous infarction as one or more migraine aura symptoms associated with an ischemic brain lesion in a correlating anatomical clinical territory demonstrated by neuroimaging. It should occur in a patient with a history of migraine with aura and typical of previous attacks except that one or more aura symptoms persists for more than 60 minutes, and it should not be better accounted for by another diagnosis. Clearly associating an ischemic stroke and a migraine attack in a migraine sufferer can be difficult. Cerebral infarction of other etiologies can coexist with migraine, can present with symptoms resembling migraine with aura, or cerebral infarction can occur during an attack of migraine with aura, and this is the only scenario that would be consistent with migrainous infarction.

Migrainous infarction occurs predominantly in the posterior circulation and in younger women. In the Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis (CAMERA) study, these infarct-like white matter lesions found in migraineurs (primarily in migraine with aura) were predominantly located in the posterior circulation, especially in the cerebellum. 22,23 However, these infarctions are not necessarily considered migrainous infarctions and the mechanisms are unclear.

Multiple studies have confirmed the association with increased stroke risk in women with migraine with aura. Women younger than age 45 who have migraine with aura, have a 2 fold increased risk of stroke. Notably, migraine without aura does not appear to have the same increased risk. This risk increases to 6 fold in the setting of oral contraceptive use containing estrogen, and more than 9 fold with combined smoking and oral contraceptive use. 24 Menstrual migraine and the use of hormonal therapy and birth control is discussed in more detail here. Women who are smokers and have migraine with aura should consider estrogen containing oral contraception a contraindication. Oral contraceptive use in non-smoking women with migraine with aura is more controversial. The World Health Organization (WHO) and American College of Obstetrics and Gynecology (ACOG) suggest that in non-smoking women under age 35 with migraine with aura, there is an acceptable lower risk of oral contraceptive use. However, if they are over age 35, the risk is unacceptably higher and oral contraceptive use is contraindicated. According to the International Headache Society (IHS), in non-smoking women with migraine with aura who are either younger or older than age 35, taking into account other risk factors should individualize the decision for oral contraceptives. 24 These would include ischemic heart disease, family history of early heart disease at a young age of less than 45 years old, heart disease with concern for emboli such as atrial fibrillation, uncontrolled hypertension, hyperlipidemia, diabetes, obesity, systemic disease associated with increased stroke (connective tissue disease, sickle cell, hypercoagulability), etc. In women with an increased risk of stroke, and especially with multiple vascular risk factors, non-estrogen methods of birth control such as progesterone-only forms of contraception should be recommended.

Research has also reported that after high blood pressure, migraine with aura was the second strongest single predictor of heart attack and strokes, ahead of diabetes, smoking, obesity, and family history of early heart disease. 25 This increased risk was not seen in migraine without aura. It is not necessarily thought that migraine with aura causes the stroke, but rather it is a marker for young women at a greater risk for cardiovascular disease. However, the reasons for these associations are unclear, likely multifactorial, and clearly need to be further defined. Traditional vascular risk factors such as hypertension, smoking, diabetes and hyperlipidemia still show the strongest contribution to cardiovascular disease, so these should be optimized, especially in those with migraine with aura to reduce risk of both heart disease and stroke. 25

Some theorized mechanisms of migrainous infarction include vasospasm, endothelial dysfunction, vascular endothelium-related hypercoagulability during cortical spreading depression and the aura phase, or genetic alterations of the wall of the small cerebral arterial vessel walls. 26-31

The evaluation for migrainous infarction is similar to that of persistent migraine aura without infarction. By definition, an ischemic infarct in a correlating anatomic area to symptoms should be seen on MRI or CT of the brain. This warrants a further standard stroke evaluation, including imaging of the intra and extracranial vasculature (including carotid arteries), as well as cardiac evaluations beginning with transthoracic echocardiography. Electrocardiogram and telemetry should also be pursued to evaluate for paroxysmal arrhythmias such as atrial fibrillation.

Treatment of migrainous infarction is the same as with any ischemic stroke. The initial goal is to evaluate for potentially treatable etiologies (such as cardioembolic source) and treat accordingly. Otherwise, secondary stroke risk factor modifications are the goal and include antiplatelet therapy in combination with optimal control of blood pressure, hypertension, hyperlipidemia, diabetes, tobacco cessation, and healthy lifestyle changes.

Abortive migraine options can include the gepants (Ubrelvy, Nurtec ODT), ditans (Reyvow), NSAIDs and other conventional abortives, although triptans and ergots should be avoided.



  1. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2013;33:629-808.
  2. Wolff HG. Headache and Other Head Pain. New York: Oxford University Press, 1963.
  3. Olesen J, Larsen B, Lauritzen M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann Neurol 1981;9:344-52.
  4. Lauritzen M. Pathophysiology of the migraine aura. The spreading depression theory. Brain 1994;117 ( Pt 1):199-210.
  5. Lauritzen M, Skyhoj Olsen T, Lassen NA, Paulson OB. Changes in regional cerebral blood flow during the course of classic migraine attacks. Ann Neurol 1983;13:633-41.
  6. Lauritzen M,  Olesen J. Regional cerebral blood flow during migraine attacks by Xenon-133 inhalation and emission tomography. Brain 1984;107 ( Pt 2):447-61.
  7. Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neurol Psych. 1941;46:331-339.
  8. Leao AAP. Spreading depression of activity in cerebral cortex. Journal of Neurophysiology 1944;7:359-390.
  9. Leao AAP,  Morrison RS. Propagation of spreading cortical depression. Journal of Neurophysiology 1945;8:33-45.
  10. Leao AAP. Pial circulation and spreading depression of activity in the cerebral cortex. Journal of Neurophysiology 1944;7:391-396.
  11. Thomsen LL, Iversen HK, Olesen J. Cerebral blood flow velocities are reduced during attacks of unilateral migraine without aura. Cephalalgia 1995;15:109-16.
  12. Kobari M, Meyer JS, Ichijo M, Kawamura J. Cortical and subcortical hyperperfusion during migraine and cluster headache measured by Xe CT-CBF. Neuroradiology 1990;32:4-11.
  13. Sakai F,  Meyer JS. Regional cerebral hemodynamics during migraine and cluster headaches measured by the 133Xe inhalation method. Headache 1978;18:122-32.
  14. Tfelt-Hansen PC,  Koehler PJ. One hundred years of migraine research: major clinical and scientific observations from 1910 to 2010. Headache 2011;51:752-78.
  15. Moskowitz MA. Neurogenic inflammation in the pathophysiology and treatment of migraine. Neurology 1993;43:S16-20.
  16. Thissen S, Vos IG, Schreuder TH, Schreurs WM, Postma LA, Koehler PJ. Persistent migraine aura: new cases, a literature review, and ideas about pathophysiology. Headache 2014;54:1290-309.
  17. Relja G, Granato A, Ukmar M, Ferretti G, Antonello RM, Zorzon M. Persistent aura without infarction: decription of the first case studied with both brain SPECT and perfusion MRI. Cephalalgia 2005;25:56-9.
  18. Chen WT, Lin YY, Fuh JL, Hamalainen MS, Ko YC, Wang SJ. Sustained visual cortex hyperexcitability in migraine with persistent visual aura. Brain 2011;134:2387-95.
  19. Wang YF, Fuh JL, Chen WT, Wang SJ. The visual aura rating scale as an outcome predictor for persistent visual aura without infarction. Cephalalgia 2008;28:1298-304.
  20. Chronicle E,  Mulleners W. Might migraine damage the brain? Cephalalgia 1994;14:415-8.
  21. Coppola G, Parisi V, Di Lorenzo C, et al. Lateral inhibition in visual cortex of migraine patients between attacks. J Headache Pain 2013;14:20,2377-14-20.
  22. Kruit MC, van Buchem MA, Launer LJ, Terwindt GM, Ferrari MD. Migraine is associated with an increased risk of deep white matter lesions, subclinical posterior circulation infarcts and brain iron accumulation: the population-based MRI CAMERA study. Cephalalgia 2010;30:129-36.
  23. Kruit MC, Launer LJ, Ferrari MD, van Buchem MA. Infarcts in the posterior circulation territory in migraine. The population-based MRI CAMERA study. Brain 2005;128:2068-77.
  24. Tepper SJ, Tepper DE. The Cleveland Clinic Manual of Headache Therapy, 2nd ed. . Switzerland: Springer International Publishing, 2014.
  25. Kurth T, Bubes V, Buring J. Relative Contribution of Migraine with Aura to Cardiovascular Disease Occurrence in Women. Neurology 2013;80.
  26. Pezzini A, Del Zotto E, Giossi A, et al. The migraine-ischemic stroke relation in young adults. Stroke Res Treat 2010;2011:304921.
  27. Pezzini A, Del Zotto E, Giossi A, Volonghi I, Grassi M, Padovani A. The migraine-ischemic stroke connection: potential pathogenic mechanisms. Curr Mol Med 2009;9:215-26.
  28. Kurth T, Chabriat H, Bousser MG. Migraine and stroke: a complex association with clinical implications. Lancet Neurol 2012;11:92-100.
  29. Kurth T. Migraine and ischaemic vascular events. Cephalalgia 2007;27:965-75.
  30. Tietjen EG. Migraine and ischaemic heart disease and stroke: potential mechanisms and treatment implications. Cephalalgia 2007;27:981-7.
  31. Bousser MG,  Welch KM. Relation between migraine and stroke. Lancet Neurol 2005;4:533-42.

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Last updated on October 22nd, 2020 at 12:14 am





Chronic daily headache being endlessly fueled and driven by rebound headache (medication overuse headache or MOH) is one of the most common headache disorders that headache specialists encounter every day in clinic. Chronic daily headache refers to 15-30 days of headache per month on average for 3 or more months. The most common cause of chronic daily headache is typically chronic migraine, in which at least 8 days out of those 15-30 days per month have migrainous characteristics (throbbiness, throbby, pounding, pulsating pain with nausea and/or sensitivity to light (photophobia) and sound (phonophobia)).


Patients that have a prior or current history of headaches such as migraine or tension-type headaches tend to be highly susceptible to developing rebound headache/MOH when certain medications are being used too frequently, but it predominantly occurs in patients with a history of migraine. The overused medications may be actively used for headache (usually the case), but they may also be used for something entirely different such as back pain, nerve pain, arthritis pain, or anything else. The reason these medications are being used doesn’t matter as much as the frequency that they are being used. When certain medications are used too frequently, it will inadvertently cause the patient’s prior migraines to emerge and begin to increase in frequency and severity until it eventually evolves over time into a chronic daily headache with worsening severity. Once someone is stuck in the rut of chronic daily headache from chronic migraine and rebound headache/MOH, it can be very challenging to pull them back out of this cycle, and the rebound/MOH must be eliminated before improvement can occur. In addition, preventative medications (daily medicines used to lessen the frequency and/or severity of headaches) and abortive (“as-needed” at headache onset) pain medications generally become less effective in the setting of rebound/MOH.


Research has shown that medication overuse can transform episodic migraine (0-15 days of headache per month) to chronic migraine (15-30 days of headache per month) if the following medications are used at the following frequencies:

Greater than 10 days per month for 2 or more consecutive months of over the counter (OTC) pain medications (Tylenol, Excedrin, Acetaminophen, Aleve, Naproxen, Motrin, Advil, Ibuprofen, or other non-steroidal anti-inflammatories (NSAIDs)).

Greater than 10 days per month for 2 or more consecutive months of triptans (Sumatriptan, Rizatriptan, Zolmitriptan, Almotriptan, Frovatriptan, Naratriptan, Eletriptan).

Greater than 8 days per month for 2 or more months of any narcotic, opioid, or opiate medication (Vicodin, Norco, Hydrocodone, Oxycodone, Oxycontin, Percocet, Tramadol, Ultram, Ultracet, Morphine, Codeine, Dilaudid, etc.).

Greater than 5 days per month for 2 or more months of any butalbital containing medication (Fioricet, Fiorinal, Esgic); (also known as “the headache specialist’s worst enemy”).


The chronic daily headaches will never improve until a weaning detoxification from the overused medications happens. It can take up to 6-12 weeks for improvement to start to occur beginning after there is a consistent detoxification and minimizing use of the offending medication. This time-frame may vary depending on the medicine used, duration of use, frequency of use, and quantity of use. It is also important to know that as the patient is weaning and detoxing from the overused medications, headaches will commonly get worse (rebound) before they get better. The hardest part of breaking out of this cycle can be getting through that rebound hump. Unfortunately, there is not typically a “quick fix” for this scenario.


This process of weaning and detoxification is generally accompanied by starting and adjusting preventative daily headache medications by the patient’s physician. A general slow wean off of overused medications is seen below, and can be adjusted based on quantity and frequency of the overused medication:

Week 1: If using daily, decrease to half of the amount of medication typically used daily (for example, if taking Tylenol 4 times per day, decrease to 2 times per day, etc.).
Week 2: Use no more than 6 days per week.
Week 3: Use no more than 5 days per week.
Week 4: Use no more than 4 days per week.
Week 5: Use no more than 3 days per week.
Week 6: Use no more than 2 days per week or less.


Some people prefer to get through this weaning process faster rather than a slow wean such as this. Some choose to stop their overused medications “cold turkey” to expedite the process. This should be discussed with your physician because it can be medically unsafe to abruptly stop some medications such as fioricet, fiorinal, butalbital, opioids and opiates which can result in seizures, irregular heart rhythms, blood pressure changes, or other withdrawal syndromes. A “bridging” medication to help “bridge” out of this cycle is often used, or provided as a rescue to save for use during a slow wean to take if the rebound headache becomes intolerable. These bridging rescue medications may include a course of steroids, NSAIDs, IV infusions, or many other options depending on what medicine is being weaned and other medical conditions present. The bottom line is that it can be a painful, frustrating, and challenging process to pull out of a rebound/MOH cycle. So hang in there and stick with it because once you successfully get out of this rut, you’ll be happy you did!

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Last updated on October 20th, 2020 at 06:53 am




Chiari malformation is a common anatomical variation, specifically type I which this blog summarizes. It is most often a benign and asymptomatic finding found incidentally during routine imaging of the brain when an MRI or CT is done for other reasons, including headache. The difficulty is often trying to associate the likelihood of a patient’s symptoms with the Chiari malformation. Internet searching will give you a very long list of reported symptoms caused by Chiari malformation, many of which are inaccurate. Chiari malformation that is truly related to a patient’s symptoms typically include a “pegged” appearance of the cerebellar tonsils (back and bottom part of the cerebellum) which are pointed rather than rounded, suggesting compression at the cervicomedullary junction (area where the brainstem and upper cervical spinal cord merge between the bottom of the skull and upper cervical spine). When this appearance is present, the patient often does have symptoms that correlate to the Chiari. Unfortunately, most of the time the Chiari malformation is not as extensive, making it more difficult to determine if some of the patient’s symptoms are correlated or not. A contrast brain MRI which includes a cine flow (cine-phase contrast) study can be helpful in determining the extent of compression and subsequent blockage of normal cerebrospinal fluid (CSF) flow throughout the craniocervical junction. A cervical MRI without contrast is also recommended to rule out a cervical syrinx (enlarged area in the center of the spinal cord), which can sometimes be associated with Chiari. If a cervical syrinx is found, an MRI of the remaining thoracic and lumbar spine should also be performed.

Reference: “When Your Brain is Falling Out: My Chiari Diagnosis” – diaryofafitmommy.com

In general, Chiari malformation cerebellar tonsillar herniation is considered to be within normal anatomical variation in the following:
-First decade (0-10 years): 6mm or less
-Second and third decades (10-30 years): 5mm or less
-Fourth-eighth decades (30 to 80 years): 4mm or less
-Ninth decade (greater than 80 years): 3mm or less


Some mild or borderline Chiari malformations can be associated with extensive symptoms, while other times an extensive Chiari malformation is found, but the patient lacks any Chiari symptoms. So, a detailed history of symptoms including headache and associated features is crucial in determining whether a Chiari malformation is clinically relevant or not. This is more useful than basing treatment decisions purely on the extent of tonsillar herniation in Chiari. History is also important in excluding other disorders which can cause a reversible “pseudo-Chiari”, caused by a different disorder such as intracranial hypotension CSF leak, or low-pressure headache) or idiopathic intracranial hypertension (IIH) (previously known as pseudotumor cerebri).


According to the International Classification of Headache Disorders 3rd Edition (ICHD3), Chiari headache caused by Chiari type I malformation is usually occipital or suboccipital, of short duration (less than 5 minutes) and provoked by cough or other Valsalva-like maneuvers (straining in the abdominal region such as when having a bowel movement). It remits after the successful treatment of the Chiari malformation.


Diagnostic criteria require Chiari malformation to have at least two of the following:

1. Either or both of the following:
a) Headache has developed in temporal relation to the Chiari or led to its discovery
b) Headache has resolved within 3 months after successful treatment of the Chiari


2. Headache has one or more of the following three characteristics:
a) Precipitated by cough or other Valsalva-like maneuver
b) Occipital or suboccipital location
c) Lasting less than 5 minutes


3. Headache is associated with other symptoms and/or clinical signs of brainstem, cerebellar, lower cranial nerve and/or cervical spinal cord dysfunction. (These may include symptoms such as hoarseness, slurred speech, swallowing or choking difficulty, unsteadiness, dizziness, vertigo, tongue weakness, trigeminal or glossopharyngeal neuralgia, tinnitus, absent gag reflex, facial numbness, autonomic symptoms (syncope, slow heart rate (bradycardia), drop attacks), loss of pain and temperature sensation of the upper torso and arms (from syrinx), loss of muscle strength in the hands and arms (from syrinx)


According to ICHD3 criteria, diagnosis of Chiari malformation by MRI requires a 5-mm caudal descent of the cerebellar tonsils or 3-mm caudal descent of the cerebellar tonsils plus crowding of the subarachnoid space at the craniocervical junction as evidenced by compression of the CSF spaces posterior and lateral to the cerebellum, or reduced height of the supraocciput, or increased slope of the tentorium, or kinking of the medulla oblongata.


Unfortunately, we see many patients who have had Chiari decompression, but they continue to have chronic daily headache which often resembles their pre-surgery headaches. When you delve deeper into their pre-existing headaches, many times they describe headaches which had/have migrainous features (throbbing, pounding, pulsating pain quality with nausea (+/- vomiting) and/or photophobia and phonophobia (sensitivity to bright light and loud sound with bad headache flares)). Many times, the chronic daily headaches that patients continue to have after surgery are associated with some variable degree of these migrainous characteristics. Overall, they typically resemble a chronic migraine pattern, and many times treating the headaches as chronic migraine rather than being distracted and treating only as ongoing Chiari headache can provide significant improvement. Even more important is screening for these migrainous features prior to surgery, and if present, treatments targeting migraine and chronic migraine should always be exhausted first because pure Chiari headache is not going to cause migrainous features of throbbing, pounding, pulsating headache with nausea (+/- vomiting) and/or photophobia and phonophobia.


In addition to a chronic migraine appearing headache, patients who have had Chiari decompression frequently have associated occipital neuralgia (see education pages) in the back of the head and a component of chronic post-craniotomy headache. Post-craniotomy headache is technically similar to chronic post-traumatic headache since surgery is, well, certainly a form of trauma to the head. Chronic post-traumatic headache itself commonly has a chronic migraine clinical appearance (with or without pre-existing migraine history), and treating as such can often be very beneficial.


Successful treatment with significant improvement of chronic daily headache with chronic migraine characteristics following Chiari decompression surgery is often a difficult task requiring patience and a good headache specialist. Onabotulinum toxin A (as of 2010, still the only FDA approved chronic migraine treatment), according to the PREEMPT protocol with some additional dosing over the occipital nerves is often helpful. Daily medications used in migraine prevention can also be helpful, particularly ones that are good for not only migraine, but also occipital neuralgia and musculoskeletal pain such as anticonvulsants (topiramate, gabapentin, etc.), TCAs (amitriptyline, nortriptyline), or SNRIs (duloxetine, venlafaxine ER). Ensuring there is no ongoing chronic daily headache driver from rebound headache (medication overuse headache) is also crucial to improvement.

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