What happens in my brain when I get a migraine? And what medications can I use to treat it?

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Migraine is many things, but one thing it’s not is “just a headache”.

“Migraine” comes from the Greek word “hemicrania”, referring to the common experience of migraine being predominantly one-sided.

Some people experience an “aura” preceding the headache phase – usually a visual or sensory experience that evolves over five to 60 minutes. Auras can also involve other domains such as language, smell and limb function.

Migraine is a disease with a huge personal and societal impact. Most people cannot function at their usual level during a migraine, and anticipation of the next attack can affect productivity, relationships and a person’s mental health.

Francisco Gonzelez/Unsplash

What’s happening in my brain?

The biological basis of migraine is complex, and varies according to the phase of the migraine. Put simply:

The earliest phase is called the prodrome. This is associated with activation of a part of the brain called the hypothalamus which is thought to contribute to many symptoms such as nausea, changes in appetite and blurred vision.

The hypothalamus is shown here in red. Blamb/Shutterstock

Next is the aura phase, when a wave of neurochemical changes occur across the surface of the brain (the cortex) at a rate of 3–4 millimetres per minute. This explains how usually a person’s aura progresses over time. People often experience sensory disturbances such as flashes of light or tingling in their face or hands.

In the headache phase, the trigeminal nerve system is activated. This gives sensation to one side of the face, head and upper neck, leading to release of proteins such as CGRP (calcitonin gene-related peptide). This causes inflammation and dilation of blood vessels, which is the basis for the severe throbbing pain associated with the headache.

Finally, the postdromal phase occurs after the headache resolves and commonly involves changes in mood and energy.

What can you do about the acute attack?

A useful way to conceive of migraine treatment is to compare putting out campfires with bushfires. Medications are much more successful when applied at the earliest opportunity (the campfire). When the attack is fully evolved (into a bushfire), medications have a much more modest effect.

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Aspirin

For people with mild migraine, non-specific anti-inflammatory medications such as high-dose aspirin, or standard dose non-steroidal medications (NSAIDS) can be very helpful. Their effectiveness is often enhanced with the use of an anti-nausea medication.

Triptans

For moderate to severe attacks, the mainstay of treatment is a class of medications called “triptans”. These act by reducing blood vessel dilation and reducing the release of inflammatory chemicals.

Triptans vary by their route of administration (tablets, wafers, injections, nasal sprays) and by their time to onset and duration of action.

The choice of a triptan depends on many factors including whether nausea and vomiting is prominent (consider a dissolving wafer or an injection) or patient tolerability (consider choosing one with a slower onset and offset of action).

As triptans constrict blood vessels, they should be used with caution (or not used) in patients with known heart disease or previous stroke.

Nurse takes blood pressure
Triptans should be used cautiously in patients with heart disease. CDC/Unsplash

Gepants

Some medications that block or modulate the release of CGRP, which are used for migraine prevention (which we’ll discuss in more detail below), also have evidence of benefit in treating the acute attack. This class of medication is known as the “gepants”.

Gepants come in the form of injectable proteins (monoclonal antibodies, used for migraine prevention) or as oral medication (for example, rimegepant) for the acute attack when a person has not responded adequately to previous trials of several triptans or is intolerant of them.

They do not cause blood vessel constriction and can be used in patients with heart disease or previous stroke.

Ditans

Another class of medication, the “ditans” (for example, lasmiditan) have been approved overseas for the acute treatment of migraine. Ditans work through changing a form of serotonin receptor involved in the brain chemical changes associated with the acute attack.

However, neither the gepants nor the ditans are available through the Pharmaceutical Benefits Scheme (PBS) for the acute attack, so users must pay out-of-pocket, at a cost of approximately A$300 for eight wafers.

What about preventing migraines?

The first step is to see if lifestyle changes can reduce migraine frequency. This can include improving sleep habits, routine meal schedules, regular exercise, limiting caffeine intake and avoiding triggers such as stress or alcohol.

Despite these efforts, many people continue to have frequent migraines that can’t be managed by acute therapies alone. The choice of when to start preventive treatment varies for each person and how inclined they are to taking regular medication. Those who suffer disabling symptoms or experience more than a few migraines a month benefit the most from starting preventives.

Pharmacy assistant serves customer
Some people will take medicines to prevent migraines. Tbel Abuseridze/Unsplash

Almost all migraine preventives have existing roles in treating other medical conditions, and the physician would commonly recommend drugs that can also help manage any pre-existing conditions. First-line preventives include:

  • tablets that lower blood pressure (candesartan, metoprolol, propranolol)
  • antidepressants (amitriptyline, venlafaxine)
  • anticonvulsants (sodium valproate, topiramate).

Some people have none of these other conditions and can safely start medications for migraine prophylaxis alone.

For all migraine preventives, a key principle is starting at a low dose and increasing gradually. This approach makes them more tolerable and it’s often several weeks or months until an effective dose (usually 2- to 3-times the starting dose) is reached.

It is rare for noticeable benefits to be seen immediately, but with time these drugs typically reduce migraine frequency by 50% or more.


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‘Nothing works for me!’

In people who didn’t see any effect of (or couldn’t tolerate) first-line preventives, new medications have been available on the PBS since 2020. These medications block the action of CGRP.

The most common PBS-listed anti-CGRP medications are injectable proteins called monoclonal antibodies (for example, galcanezumab and fremanezumab), and are self-administered by monthly injections.

These drugs have quickly become a game-changer for those with intractable migraines. The convenience of these injectables contrast with botulinum toxin injections (also effective and PBS-listed for chronic migraine) which must be administered by a trained specialist.

Up to half of adolescents and one-third of young adults are needle-phobic. If this includes you, tablet-form CGRP antagonists for migraine prevention are hopefully not far away.

Data over the past five years suggest anti-CGRP medications are safe, effective and at least as well tolerated as traditional preventives.

Nonetheless, these are used only after a number of cheaper and more readily available first-line treatments (all which have decades of safety data) have failed, and this also a criterion for their use under the PBS.

Mark Slee, Associate Professor, Clinical Academic Neurologist, Flinders University and Anthony Khoo, Lecturer, Flinders University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • Who Will Take Care of Me When I’m Old? – by Joy Loverde

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    Regular readers of 10almonds will know we’ve written before about how isolation kills (in numerous ways), and this book tackles that in much greater length and depth than we ever have room for here.

    Specifically, she talks about preparing for medical and related (financial, living will in case of dementia, housing, etc) considerations down the line, with checklists and worksheets and such to make it easy, and help you make sure it actually gets done.

    She also talks about creating a support network, from scratch if necessary (“foraging a family”), so that even if you will now be prepared to handle things alone, you’ll become a lot less likely to need to do so.

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  • Aspirin, CVD Risk, & Potential Counter-Risks

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    Aspirin Pros & Cons

    In Tuesday’s newsletter, we asked your health-related opinion of aspirin, and got the above-depicted, below-described set of responses:

    • About 42% said “Most people can benefit from low-dose daily use to lower CVD risk”
    • About 31% said “It’s safe for occasional use as a mild analgesic, but that’s all”
    • About 28% said “We should avoid aspirin; it can cause liver and/or kidney damage”

    So, what does the science say?

    Most people can benefit from low-dose daily aspirin use to lower the risk of cardiovascular disease: True or False?

    True or False depending on what we mean by “benefit from”. You see, it works by inhibiting platelet function, which means it simultaneously:

    • decreases the risk of atherothrombosis
    • increases the risk of bleeding, especially in the gastrointestinal tract

    When it comes to balancing these things and deciding whether the benefit merits the risk, you might be asking yourself: “which am I most likely to die from?” and the answer is: neither

    While aspirin is associated with a significant improvement in cardiovascular disease outcomes in total, it is not significantly associated with reductions in cardiovascular disease mortality or all-cause mortality.

    In other words: speaking in statistical generalizations of course, it may improve your recovery from minor cardiac events but is unlikely to help against fatal ones

    The current prevailing professional (amongst cardiologists) consensus is that it may be recommended for secondary prevention of ASCVD (i.e. if you have a history of CVD), but not for primary prevention (i.e. if you have no history of CVD). Note: this means personal history, not family history.

    In the words of the Journal of the American College of Cardiology:

    ❝Low-dose aspirin (75-100 mg orally daily) might be considered for the primary prevention of ASCVD among select adults 40 to 70 years of age who are at higher ASCVD risk but not at increased bleeding risk (S4.6-1–S4.6-8).

    Low-dose aspirin (75-100 mg orally daily) should not be administered on a routine basis for the primary prevention of ASCVD among adults >70 years of age (S4.6-9).

    Low-dose aspirin (75-100 mg orally daily) should not be administered for the primary prevention of ASCVD among adults of any age who are at increased risk of bleeding (S4.6-10).❞

    ~ Dr. Donna Arnett et al. (those section references are where you can find this information in the document)

    Read in full: Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology

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    Many older adults still use aspirin for CVD prevention, contrary to clinical guidance

    Aspirin can cause liver and/or kidney damage: True or False?

    True, but that doesn’t mean we must necessarily abstain, so much as exercise caution.

    Aspirin is (at recommended doses) not usually hepatotoxic (toxic to the liver), but there is a strong association between aspirin use in children and the development of Reye’s syndrome, a disease involving encephalopathy and a fatty liver. For this reason, most places have an official recommendation that aspirin not be used by children (cut-off age varies from place to place, for example 12 in the US and 16 in the UK, but the key idea is: it’s potentially dangerous for those who are not fully grown).

    Aspirin is well-established as nephrotoxic (toxic to the kidneys), however, the toxicity is sufficiently low that this is not expected to be a problem to otherwise healthy adults taking it at no more than the recommended dose.

    For numbers, symptoms, and treatment, see this very clear and helpful resource:

    An evidence based flowchart to guide the management of acute salicylate (aspirin) overdose

    Take care!

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  • How to Find Happiness In Yourself – by Michelle Mann

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    A lot of books about happiness tell you what to pursue, generally. What things to focus on, and that’s good, but incomplete. This book does cover those things too (complete with academic sources to back up what really works), but also goes further:

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  • The Real Benefit Of Genetic Testing

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    Genetic Testing: Health Benefits & Methods

    Genetic testing is an oft-derided American pastime, but there’s a lot more to it than finding out about your ancestry!

    Note: because there are relatively few companies offering health-related genetic testing services, and we are talking about the benefits of those services, some of this main feature may seem like an advert.

    It’s not; none of those companies are sponsoring us, and if any of them become a sponsor at some point, we’ll make it clear and put it in the clearly-marked sponsor segment.

    As ever, our only goal here is to provide science-backed information, to enable you to make your own, well-informed, decisions.

    Health genomics & genetic testing

    The basic goal of health genomics and genetic testing is to learn:

    • What genetic conditions you have
      • Clearcut genetic conditions, such as Fragile X syndrome, or Huntington’s disease
    • What genetic predispositions you have
      • Such as an increased/decreased risk for various kinds of cancer, diabetes, heart conditions, and so forth
    • What genetic traits you have
      • These may range from “blue eyes” to “superathlete muscle type”
    • More specifically, pharmacogenomic information
      • For example, “fast caffeine metabolizer” or “clopidogrel (Plavix) non-responder” (i.e., that drug simply will not work for you)

    Wait, what’s the difference between health genomics and genetic testing?

    • Health genomics is the science of how our genes affect our health.
    • Genetic testing can be broadly defined as the means of finding out which genes we have.

    A quick snippet…

    More specifically, a lot of these services look at which single nucleotide polymorphisms (SNPs, pronounced “snips”) we have. While we share almost all of our DNA with each other (and indeed, with most vertebrates), our polymorphisms are the bits that differ, and are the bits that, genetically speaking, make us different.

    So, by looking just at the SNPs, it means we “only” need to look at about 3,000,000 DNA positions, and not our entire genome. For perspective, those 3,000,000 DNA positions make up about 0.1% of our whole genome, so without focusing on SNPs, the task would be 1000x harder.

    For example, the kind of information that this sort of testing may give you, includes (to look at some “popular” SNPs):

    • rs53576 in the oxytocin receptor influences social behavior and personality
    • rs7412 and rs429358 can raise the risk of Alzheimer’s disease by more than 10x
    • rs6152 can influence baldness
    • rs333 resistance to HIV
    • rs1800497 in a dopamine receptor may influence the sense of pleasure
    • rs1805007 determines red hair and sensitivity to anesthetics
    • rs9939609 triggers obesity and type-2 diabetes
    • rs662799 prevents weight gain from high fat diets
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    • rs1799971 makes alcohol cravings stronger
    • rs17822931 determines earwax, sweating and body odor
    • rs1333049 coronary heart disease
    • rs1051730 and rs3750344 nicotine dependence
    • rs4988235 lactose intolerance

    (You can learn about these and more than 100,000 other SNPs at SNPedia.com)

    I don’t know what SNPs I have, and am disinclined to look them up one by one!

    The first step to knowing, is to get your DNA out of your body and into a genetic testing service. This is usually done by saliva or blood sample. This writer got hers done many years ago by 23andMe and was very happy with that service, but there are plenty of other options.

    Healthline did an independent review of the most popular companies, so you might like to check out:

    Healthline: Best DNA Testing Kits of 2023

    Those companies will give you some basic information, such as “6x higher breast cancer risk” or “3x lower age-related macular degeneration risk” etc.

    However, to really get bang-for-buck, what you want to do next is:

    1. Get your raw genetic data (the companies above should provide it); this will probably look like a big text file full of As, Cs, Gs, and Ts, but it make take another form.
    2. Upload it to Promethease. When this writer got hers done , the cost was $2; that price has now gone up to a whopping $12.
    3. You will then get a report that will cross-reference your data with everything known about SNPs, and give a supremely comprehensive, readable-to-the-human-eye, explanation of what it all means for you—from much more specific health risk prognostics, to more trivial things like whether you can roll your tongue or smell decomposed asparagus metabolites in urine.

    A note on privacy: anything you upload to Promethease will be anonymized, and/but in doing so, you consent to it going into the grand scientific open-source bank of “things we know about the human genome”, and thus contribute to the overall sample size of genetic data.

    In our opinion, it means you’re doing your bit for science, without personal risk. But your opinion may differ, and that’s your decision to make.

    Lastly, on the pros and cons of pharmacogenetic testing specifically:

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  • Top 5 Anti-Aging Exercises

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    There are some exercises that get called such things as “The King of Exercises!”, but how well-earned is that title and could it be that actually a mix of the top few is best?

    The Exercises

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    • Glute Bridges: this nicely rounds off one’s core strength, increasing stability and improving posture, as well as reducing lower back pain too.

    If the benefits of these seem to overlap a little, it’s because they do! But each does some things that the others don’t, so put together, they make for a very well-balanced workout.

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    Click Here If The Embedded Video Doesn’t Load Automatically!

    Want to learn more?

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    Take care!

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  • Sweet Dreams Are Made Of Cheese (Or Are They?)

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    It’s Q&A Day at 10almonds!

    Have a question or a request? You can always hit “reply” to any of our emails, or use the feedback widget at the bottom!

    In cases where we’ve already covered something, we might link to what we wrote before, but will always be happy to revisit any of our topics again in the future too—there’s always more to say!

    As ever: if the question/request can be answered briefly, we’ll do it here in our Q&A Thursday edition. If not, we’ll make a main feature of it shortly afterwards!

    So, no question/request too big or small

    ❝In order to lose a little weight I have cut out cheese from my diet – and am finding that I am sleeping better. Would be interested in your views on cheese and sleep, and whether some types of cheese are worse for sleep than others. I don’t want to give up cheese entirely!❞

    In principle, there’s nothing in cheese that, biochemically, should impair sleep. If anything, its tryptophan content could aid good sleep.

    Tryptophan is found in many foods, including cheese, which (of common foods, anyway), for example cheddar cheese ranks second only to pumpkin seeds in tryptophan content.

    Tryptophan can be converted by the body into 5-HTP, which you’ve maybe seen sold as a supplement. Its full name is 5-hydroxytryptophan.

    5-HTP can, in turn, be used to make melatonin and/or serotonin. Which of those you will get more of, depends on what your body is being cued to do by ambient light/darkness, and other environmental cues.

    If you are having cheese and then checking your phone, for instance, or otherwise hanging out where there are white/blue lights, then your body may dutifully convert the tryptophan into serotonin (calm wakefulness) instead of melatonin (drowsiness and sleep).

    In short: the cheese will (in terms of this biochemical pathway, anyway) augment some sleep-inducing or wakefulness-inducing cues, depending on which are available.

    You may be wondering: what about casein?

    Casein is oft-touted as producing deep sleep, or disturbed sleep, or vivid dreams, or bad dreams. There’s no science to back any of this up, though the following research review is fascinating:

    Dreams of the Rarebit Fiend: food and diet as instigators of bizarre and disturbing dreams

    (it largely supports the null hypothesis of “not a causal factor” but does look at the many more likely alternative explanations, ranging from associated actually casual factors (such as alcohol and caffeine) and placebo/nocebo effect)

    Finally, simple digestive issues may be the real thing at hand:

    Association between digestive symptoms and sleep disturbance: a cross-sectional community-based study

    Worth noting that around two thirds of all people, including those who regularly enjoy dairy products, have some degree of lactose intolerance:

    Lactose Intolerance in Adults: Biological Mechanism and Dietary Management

    So, in terms of what cheese may be better/worse for you in this context, you might try experimenting with lactose-free cheese, which will help you identify whether that was the issue!

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