On 7 November 2024, we held a webinar for Migraine Foundation Aotearoa New Zealand members with neurologist Dr Ray Bose, following on from the webinar with Dr Rosamund Hill on 21 May. We had more questions from members about all things migraine.
We’ve summarised some highlights below. We’d like to share the full video recording on our website at some point but currently lack the technical capacity. (If anyone has expertise in video editing, please get in touch.)
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Here are some of the Q&As from the session with Dr Bose.
Many in our community listened to your interview on Radio New Zealand a couple of months ago about neuroimaging and migraine. Can you give us a brief recap on brain imaging in people with migraine and what they show about the nature of migraine?
Clinically when we think about migraine, there are four phases. You have the aura phase where people have symptoms like blurring of vision or zigzag lines. You have the premonitory phase where people can get cravings or a stiff neck. You have the migraine headache phase where people actually have the pain and then you have the postdrome which is the ‘hangover’ phase, where people feel tired and make a recovery from the migraine attack.
From a study on the premonitory phase of migraine, you can see areas of the brain that are lighting up on a functional MRI scan. Essentially in those areas of the brain, the nerve cells are firing. One thing that we notice in this study is that the brains of people who were on preventives did not light up. When preventive medications were working, that had a protective effect on the brain.
What do findings such as white matter hyperintensities on MRI scans mean for people with migraine?
People with migraine usually have a mild range of this white matter hyperintensity and what that means is you can see these white spots on the MRI scan – the blood vessels appear bright. What causes that in migraine? We don’t actually know. When there are moderate or severe versions of it, that is more often in older individuals or people with risk factors like high cholesterol or blood pressure.
In migraine, we don’t have any treatment for it. We just see it’s a common finding. But if we see moderate or severe forms of it, then what we tell people is to make sure that they follow a healthy diet, monitor their cholesterol and blood sugar. But there is no specific treatment to kind of reverse the hyperintensities. It can sometimes make people very anxious, but it’s quite a common finding in migraine patients and I wouldn’t worry too much about that. I would just focus on treating the migraine and making sure people have a healthy lifestyle.
We do have people in our migraine community who really want to get an MRI and check things out. But are MRIs more to rule out anything else rather than inform treatment or change the treatment?
These slides that I showed, they are very specialised MRI scans. They are not the normal MRI scans that people in a clinic or hospital have access to, so you have to be in a research study to get those kind of scans. So a typical MRI scan usually does not pick up anything on migraine. It doesn’t mean that there’s nothing there. It just means that that technology is not fit for picking that up. So usually when in clinical practice, when neurologists do a scan, it’s to make sure that there is nothing like a brain tumour or CSF leak or something like that.
Can you talk about vestibular migraine? How is this different from just feeling a bit dizzy and woozy during a migraine attack? And how is vestibular migraine treated? Is it treated any differently than migraine with or without aura?
One problem with vestibular migraine is that it’s not been studied as much as other types of migraine. So in vestibular migraine, what happens is that the vertigo is predominant over the headache itself. So people can feel dizzy or spinning for hours or maybe even days. And that is the most bothersome symptom in vestibular migraine.
In terms of treatment, because it’s less common than other migraine, not that many studies have been undertaken. But some of the drugs that you can use include things like amitriptyline, propranolol or verapamil. There have been some studies on the CGRP therapies which may be effective but we need more research on this particular type of migraine. I tend to try the funded drugs first and then if that doesn’t work then I go down the route of Emgality.
Someone has asked, how long does it take for topiramate to be totally out of your system. My husband has been taking topiramate for years and has now been on Emgality for six months. He’s titrating off the topiramate. And we’d like to know when he can be sure that it’s only Emgality acting in his system.
To know how long it will take for the drug to be completely out of the body, one needs to know something called the t half life of that drug. There is no hard and fast rule about this and so many factors can make this value variable. For example, with topiramate the fat content in your diet can affect the absorption and the levels. But to keep it simple, it takes about 8 hours for the drug to reach half its level. So we can calculate that it will be five half lives for the drug to be completely out – so 40 hours from the last dose of topiramate, it’s out of your body (8 hours times 5 half lives).
And in terms of side effects, is Emgality or topiramate better to be using long term?
Generally speaking, the tolerability of Emgality is higher than some of these older oral preventives. But everyone is different, so it can be hard to predict. I generally find that people stay on Emgality more than topiramate, but of course I’ve had people who have had side effects to Emgality and had to come off Emgality. So the general rule is that more people tolerate Emgality better, but you know there will also be some who can’t. So far we haven’t identified any kind of major long term issues with Emgality.
Next question is: I have migraine and last year I found out I had hypermobile type Ehlers-Danlos syndrome (EDS). I’m interested in migraine management and hypermobile Ehlers-Danlos syndrome. Also interested if neurologists take into consideration the possibility of this diagnosis when they’re assessing a new patient. Can you briefly explain what Ehlers-Danlos syndrome is and the correlation between migraine and if someone is diagnosed with EDS, how that changes treatment.
So Ehlers-Danlos syndrome. It’s not common. It’s a connective tissue disorder. It can affect several systems. It can affect the joints, the brain – multiple systems can get affected Depending on the type, EDS can vary between one in 10,000 or one in 50,000. So it is relatively rare compared to migraine. Headache and Ehlers-Danlos syndrome is a bit more complex, so people with EDS may have migraine, but there could be other causes for the headache as well. So you can get cervical [spine] instability causing headaches, or you could have temporomandibular joint dysfunction causing facial pain. People with Ehlers-Danlos syndrome may be at a risk of getting something called spontaneous intracranial hypertension, which is like a tear in the outer covering of the meninges of the brain causing a CSF (cerebral spinal fluid) leak. So there are multiple ways that people can get headaches in Ehlers-Danlos syndrome. I wouldn’t naturally assume a headache is migraine. I would make sure these other things are also looked into.
Talking about migraine in Ehlers-Danlos syndrome, we just treat it how we treat migraine. I would probably get an Ehlers-Danlos syndrome specialist to also give a multidisciplinary approach. All the issues must be tackled, the joint disorder and the headache disorder as well.
Do you think GPs know a lot about Ehlers-Danlos syndrome?
In general as the rarer that an illness gets, people don’t know about it. Just to give an example, cluster headache, compared to migraine cluster headache is very uncommon and there have been studies where people it sometimes takes up to five or six years before people get that diagnosis. So I think that is a problem that the rarer that an illness is, it takes longer to get diagnosed.
Atogepant has just been launched in New Zealand. If you’ve tried Emgality and that hasn’t worked for you, can you try atogepant?
The short answer is you can try atogepant if you’ve not responded to Emgality. Now, the reason being that although they do both target the CGRP mechanism, but Emgality targets the CGRP itself. So how this works is the nerve endings have CGRP. They will release CGRP, CGRP goes and binds on the CGRP receptor, activates it, and then activates the pain cascade. So Emgality goes and attacks the CGRP, the chemical or the neuropeptide itself.
Whereas the gepants, they bind on the receptor, so they stop the CGRP from coming and binding to the receptor. So even though they target CGRP, they work in slightly different ways, so if one doesn’t work, you can try the other.
One point about Emgality – from the last dose, if you stop taking it, it takes up to five months to completely clear out. Whereas atogepant, within 10 days it’s out of your body.
If they were funded, could people take both? Do people take Emgality and also atogepant?
I wouldn’t recommend it. One reason is that we’ve not studied that combination. And I’ll tell you a story. So a long time back, the CGRP drugs were in the research circles and the drug companies wanted to get these drugs out quickly. Some things that they didn’t take into account at the initial stage, especially in the US, was there were professional trial patients who were going to different sites on the same study. You know they didn’t exclude these people and they didn’t do a baseline liver function test in some of these people. And when they started analysing the results, some of the people had deranged liver function tests.
Now, they couldn’t tell whether they had pre-existing liver damage or was it because they were taking too many of these drugs, you know? So, I wouldn’t recommend taking two of them. And the other thing I want to point out is that CGRP is in the nervous system and we know that it works for migraine when we clear that. But CGRP is also in the gastrointestinal system and one of the common side effects that people get is constipation, because CGRP is probably important, and has some useful function in the gut. So I wouldn’t want to completely clear it out.
I’m very careful about constipation with Aimovig (erenumab) – not so much a problem with Emgality. People have had quite serious constipation requiring admission to ED and manual evacuation. So if people start getting quite bad constipation, despite dietary changes, I would just take them off that.
Is there a relationship between hay fever and migraine attacks? For example, can allergies set off an attack and is treatment with antihistamines effective for that?
There’s certainly an association between allergic responses and migraine. We don’t know the exact mechanisms, but probably there is a role for histamine in triggering some of the immune system responses. So if people notice a direct correlation between their allergies and migraine then taking antihistamines might be effective, but for the headache itself, the usual migraine medications might be more effective.
We hear a lot of people talk about being diagnosed with sinus headaches for years and then they actually have migraine. What’s the difference between a sinus headache and migraine?
I think that this term ‘sinus headache’ should be removed. It’s very confusing although doctors use it. Many people with ‘sinus headaches’ actually have migraine, which is easily treatable. Instead, they end up going to ENT specialists having sinuses dilated or cleared or things like that.
There are several papers which suggest that if people with so-called sinus headaches should try a triptan and see what happens rather than having invasive ENT treatment. If you have acute sinusitis or chronic sinusitis, there will be other symptoms like prominent nasal discharge, maybe pus coming out, or fever. Whereas with migraine, people can have tenderness around their sinuses, they could have a bit of autonomic symptoms and runny nose. But they would also have things like light sensitivity and sound sensitivity.
What do you advise for the treatment of migraine attacks in children or adolescents and when would you start a preventive medication?
One thing that happens with clinical trials is that they try and exclude high risk people. So they exclude children, pregnant women and older individuals. So when a drug first comes out, it’s usually been tested on someone between the age of 18 to 65.
So for that reason, the choice in children is a bit limited. It’s not saying that they’re not safe, some of the newer treatments, it’s just that we don’t have data. So at the moment in terms of preventive treatments, what are safe? Amitriptyline is probably OK. Nortriptyline, propranolol, topiramate, candesartan – these are the preventatives that you can use or probably use. Sumatriptan 50mg as well. The greater occipital nerve block I’ve used it in children and it’s also safe.
Whereas the newer treatments, like Emgality, atogepant, there are studies ongoing. Until that data comes it would be hard for kids to be prescribed them because the newer treatments, they’re not licenced for children.
Can you talk about the use of gepants for acute treatment instead of triptans? And how would that work if you were on a gepant as a preventive?
There is a gepant called rimegepant, that can be used as both a preventive medication and for treatment of a migraine attack. We don’t have this in New Zealand yet, but Australia has it.
The advantage of this is it’s the first drug that you can use both as a preventive and for acute treatment. That is unheard of in the migraine world. So normally people use a preventive and then they use a triptan for an attack. But here we have a drug that you can use for both. You take it on alternate days as a preventive and on the days in between, if you have an acute attack, you can take it.
One thing to consider with this is the cost. The drug is very expensive. And the other thing is, is it more effective than sumatriptan? Probably not. So we probably need more studies. But not everyone can have a triptan, so it’s good to have that additional choice.
But currently the only gepant we have in New Zealand is atogepant, which is just used as a preventive.
