Melbourne Headache Centre

06/06/2025

Here at the Melbourne Headache Centre, we are getting involved with Migraine Awareness Month. Studies have shown that migraine affects over 4.9 million Australians, so it’s important to us to raise awareness around Migraines, as they are often mislabelled as just a ‘bad headache’.

Our practitioners don’t just treat your symptoms, we treat the underlying disorder.

13/05/2025

After 13 years in our old location, we’ve moved to the World Trade Centre, on the city side of the Yarra River from the Convention and Exhibition Centre (a.k.a. Jeff’s Shed).

As you’re entering the World Trade Centre complex, follow the signs to the Information/Concierge Desk. You should be able to see our sign for there or ask the lovely Marwin (the concierge) for directions.

We look forward to welcoming you at our new location!

28/10/2024

Always a pleasure to be the guest of Dean and Jane Watson assisting on a Watson Headache Institute Level 1 foundation course - and Adelaide turned on magnificent whether too!

Wonderful course with a very engaging group.

Until next time.

01/05/2024

Thanks to Lee, Sheryl and the team Core Physio + Pilates for hosting me this afternoon to discuss the broader impact of the upper cervical spine in , , , , and the impact on symptoms associated with mental health disorders including and .

13/03/2024

Migraine World Summit Day 7
Inflammation & Chronic Migraine - Gretchen E. Tietjen, MD

Dr Tietjen;
"We know inflammation occurs during a migraine, but is it the cause or is it an epiphenomenon? This is being debated by Neurologists, and so it should be."

You can see both sides of the debate in my previous posts on the talks from;
Dr Robert Cowan - CGRP (part of the inflammatory process) is released in response to pain'
Prof Peter Goadsby - One of CGRP's 'roles' is it is over expressed in migraine. A finding that has not consistently been reproduced and is reflected in the low numbers having complete relief, or 75% relief with CGRP targeted medications.

Dr Tietjen;
"Neurogenic inflammation, which is often what we are talking about with migraine, you get release of neuropeptides and other inflammatory mediators, and there we're talking about things like substance P, CGRP, Neurokinin A, PACAP from the peripheral nerve endings"

A good synopsis of neurogenic inflammation - that is inflammation coming from some kind of irritation of the nerve.
It does highlight one of the key questions about the origin of increased CGRP (itself a debatable subject) which is often ascribed to the trigeminal ganglion.
CGRP and substance P are both heavily expressed from the trigeminal ganglion when irritation is induced.

In the study by Prof Goadsby that really turbo-charged the CGRP industry, substance P was not found to be elevated.

Why? This question is important, and is one that is routinely ignored as it wrecks a good story.

Goadsby, P. J., Edvinsson, L., & Ekman, R. (1990). Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Annals of Neurology, 28(2), 183–187. https://doi.org/10.1002/ana.410280213

There are many 'truths' to migraine pathogenesis. Some do have elevated CGRP, but why not substance P - what model of inflammation describes that?

Others have increased substance P and PACAP and not CGRP. Why again?

What is causing these different inflammatory cascades, and if they are epiphenomenon, targeting them is like putting water on a fire. It may help put the fire out but does not stop the next fire from starting.

So far with CGRP medications this is exactly what we see - stop taking the medications and the fire starts again.

Terhart, M., Mecklenburg, J., Neeb, L., Overeem, L. H., Siebert, A., Steinicke, M., Raffaelli, B., & Reuter, U. (2021). Deterioration of headache impact and health-related quality of life in migraine patients after cessation of preventive treatment with CGRP(-receptor) antibodies. The Journal of Headache and Pain, 22(1), 158. https://doi.org/10.1186/s10194-021-01368-7

Great that Dr Tietjen is presenting a balanced talk - there are questions. Important questions.

Dr Robert Cowan's research is;
Cowan RP, Gross NB, Sweeney MD, Sagare AP, Montagne A, Arakaki X, Fonteh AN, Zlokovic BV, Pogoda JM, Harrington MG. Evidence that blood-CSF barrier transport, but not inflammatory biomarkers, change in migraine, while CSF sVCAM1 associates with migraine frequency and CSF fibrinogen. Headache. 2021 Mar;61(3):536-545. doi: 10.1111/head.14088. Epub 2021 Mar 16. PMID: 33724462; PMCID: PMC8023403.

Dr Tietjen;
That's probably the best data set for migraine that's come out so far, and they couldn't substantiate that (i.e. didn't find elevated inflammatory markers in chronic or episodic migraine).
"That was kind of a little disconcerting."

Only if all your eggs are in the trigemino-vascular inflammation basket.
Others might view it as a great finding helping to tease out sub-groups within migraine, such as those with upper cervical pain.

Just like inflammatory conditions, some will be relevant and thers not. Discovering the true depth of the impact on upper cervical dysfunction and whether or not it is relevant to your condition relies on assessment with clinicians who have vast experience in working with migraine in all its variants and presentations.

It is a complex puzzle and rarely do simple solutions work, or last. Look for expert care to help unravel each piece of the puzzle, including the cervical spine. Contact Melbourne Headache Centre today to see if we can help unravel a piece of your puzzle.

Interview Notes Gretchen E. Tietjen, MD American Headache Society Study: “Chemokine levels in the jugular venous blood of migraine without aura patients during attacks” Study: “Endogenous glucocorticoids may serve as biomarkers for migraine chronification” Study: “Diabetes is associated wi...

11/03/2024

Migraine World Summit Day 5
Unofficial Side Effects of CGRP Monoclonal Antibodies - Robert Cowan

Always great to listen to Dr Robert Cowan. One of few willing to talk realistically about CGRP and provide scientific commentary rather than marketing. Such a contrast to Dr Goadsby on Day 2.

Dr Cowan describes CGRP is phase reactive - it goes up in response to pain.
"In migraine CGRP levels go up. They go up IN RESPONSE to pain"

He wasn't shouting that.........I'm just emphasising it because this is critical and rarely discussed. We hear fantastic stories about the genesis of migraine and CGRP's role.......CGRP isn't sitting there waiting to cause trouble. It is released in response to inflammation. In RESPONSE to.

The source of that inflammation is not something that we hear about, just what drugs should we take to deal with it.

Looking for the stressors that underly your migraine is critical to getting control over your condition. If you can tolerate the medications then by all means take them, but they are blocking the response to a probelem - not fixing the problem itself. That is why when you come off CGRP medications the migraines go back to normal frequency.

On the difference between drug trial reporting of side effects, and real world reporting;

"When we are a drug company developing a drug for migraine we want our drug to be approved. So what we do is what I call 'cherry picking' in selecting who we are going to test this on. Lets take an extreme example and say we are going to test this in people at high risk of heart attack and stroke. We know that population needs their CGRP - it's part of the healing process. Well, this drug would NEVER GET APPROVED." 😳

It should be incumbent on the pharmaceutical industry - whoever's made the drug, or the government, to catalogue these and see when that crosses the threshold, and what that threshold should be.

This talk is such a contrast to Dr Goadsby's talk on Day 2 where side effects where discussed as probably always being there, but you've just started noticing them now your headaches are gone......like you never noticed your hair falling out, your weight jumping, or being constipated until your headaches eased in frequency. 🤨

Dr Cowan mentions that CGRP plays an important role on endothelial turnover.
Unsurprisingly the main side effect from CGRP medications is GI upset, especially constipation.
Also upper respiratory infections, urinary tract infections, things that are pretty common in the general population as well.

He goes on to discuss the theoretical mechanism underlying other reported side effects, often relating to impact on micro-vasculature (hair loss, bone density), and also weight gain by modulation of insulin release.

CGRP plays an important role in our immune response and is critical to good health.

"I think we do our patients a disservice when we present drugs as being side-effect-free and being specific.
As I said CGRP is everywhere. It's hard for me to understand why it would be everywhere if it wasn't necessary. That's just not the way evolution works."

Interview Notes Robert P. Cowan, MD, FAAN, FAHS EudraVigilance (European Medicines Agency) FDA MedWatch (or 800-438-1985) Food and Drug Administration (FDA) NHS (side effect reporting) Treatments Mentioned Atogepant (Qulipta) CGRP inhibitors CGRP monoclonal antibodies (mAbs) CGRP small-molecule rece...

11/03/2024

Migraine World Summit Day 5
Migraine, TMD & Neck Pain - Rashmi B. Halker Singh

It's always interesting when Neurologists start talking about the role of the neck in migraine and even neck pain, given their general lack of training in manual therapy.

The key issue is that the neck is only considered important when there are obvious signs of structural problems as in the case of arthritis or trauma, and it is ALWAYS contingent on the presence of neck pain and loss of movement.

This ignores the fact that the most abundant sensory nerves in the neck are in fact muscle spindles from the sub occipital muscles - small changes or dysfunction affecting these muscles wreaks havoc with our sensorimotor (movement control) system, visual system, and autonomic systems (as cues from these muscles support changes in blood pressure, heart rate etc when we change posture). They are also critical to our response to threat.......anyway.....back to PAIN.

At least Dr Singh acknowledges that the nerves from the neck merge with the pathways from the trigeminal system:

"In situations where the neck pain is part of migraine we can think of it as a referred pain. These deep pain pathways have inputs from the neck, so sometimes the migraine can cause neck pain..........."

However, these pathways are bidirectional. Key studies looking at the activation of these pathways found that the same relay nerve was activated EQUALLY by stimulation of the dura in the skull OR by stimulation of upper cervical nerves.

So, yes migraine could cause neck pain........but EQUALLY valid............neck problems can cause migraine.

One of my pet bugbears with the current paradigm in migraine is how CGRP is King - despite the evidence to the contrary.
It only took 7 minutes for a CGRP 'drive-by' aimed at neck pain and TMD.

CGRP, like many other substances in the body is present in all pain syndromes - low back pain, knee arthritis, stroke, heart attacks (where it is performing a critical role to survival).
This perpetuates the 'CGRP is a migraine molecule' myth and does nothing to explain why there is an inflammatory response being initiated.

The comment on differential diagnosis here is misleading:
"If migraine attacks are discrete, whereas neck pain is all day everyday - therefore neck pain not related to migraine."

This is an overly simplistic view of a complex disorder. Migraine is a condition of accumulated stressors. You may have neck pain, inflammatory bowel disease or endometriosis. These add a significant load to your baseline stress - 'filling your cup' to 3/4 full all day......everyday. Now it is down to0 how well you navigate the other daily stressors - sleep, diet, mental/cognitive/emotional stress etc as to whether you overfill the cup and trigger an attack.

To suggest that just because something is there everyday means it doesn't play a role in an episodic disorder is silly.........and excludes any discussion about genes and migraine.

This quote encapsulates why you should seek an opinion about your neck from some who specifically deal with the role of the neck in migraine, rather than from a profession who don't understand it, and minimise its role at every turn:

"Structural problems in the neck tend to develop more as we get older, like arthritis and degenerative issues. If a 20 year old come in with no history of trauma complaining of neck pain with their migraine there's a higher chance that the neck pain is probably part of their migraine....."

Because the only cause of neck pain, or indeed neck dysfunction is degenerative disease or trauma?
Posture has no effect? Or is it that kids and teens have great posture that does not stress their neck?

We are born with large heads and weak spines. By the age of 3 we have 80% of an adult sized head. We don't develop trunk strength until our teens, putting a lot of pressure on the top of the neck. Add this to starting school, sitting most of the day and we have a huge postural loading (not to mention increases in smartphone/tablet usage).

By the age of 10 we all have demonstrable dysfunction in the upper cervical spine.

Recent research by the Melbourne Headache Centre into concussion found that at baseline (pre-injury, healthy controls) every subject tested (ages 14-28) had palpable dysfunction in the upper cervical spine.
The question is whether it is contributing significantly to your symptoms. Don't wait until you are 60 with obvious arthritis to get your Neurologist to consider your neck could be a part of the problem.

Here at the Melbourne Headache Centre we routinely see people that are in active care with a manual therapist, and even in some cases seeing other Watson Headache Practitioners, and yet the issue causing muscle spasm at C2 has not been corrected. It is rare that we cannot correct it - this is the benefit of seeing therapists who are very experienced, and understand exactly what they are looking for, and exactly what needs to happen to treat it.

Interview Notes Rashmi B. Halker Singh, MD Mayo Clinic – Arizona American Academy of Neurology American Headache Society Resident Education for Assessment and Care for Headache (REACH) Program Women’s Leadership Development Scottsdale Headache Symposium Journal: Headache American Migraine Founda...

07/03/2024

2024 Migraine World Summit - Day 2
Professor Peter Goadsby:

On CGRP
"Of its many roles, one is that it's over-expressed in migraine"

This is more accurately stated as:

CGRP is present in many chronic pain disorders including low back pain, knee osteoarthritis, and is over-expressed in SOME cases of migraine.

For example this recent paper found no elevation of CGRP in paediatric migraine patients:
Hanci, F., Kilinc, Y. B., Kilinc, E., Turay, S., Dilek, M., & Kabakus, N. (2021). Plasma levels of vasoactive neuropeptides in pediatric patients with migraine during attack and attack-free periods. Cephalalgia: An International Journal of Headache, 41(2), 166–175. https://doi.org/10.1177/0333102420957588

The original work in the 1990's by Prof Goadsby examined migraine sufferers presenting to emergency department in Australia (more severe end of migraine scale?), and compared their CGRP levels to control data from Europe (does sunlight hours impact this - Vitamin D levels have an impact on CGRP levels).
Also interesting is that the blood was draw from the external jugular vein of which 80% comes from blood outside the skull - yet the interpretation is often related to intracranial blood vessels and trigeminal ganlgion CGRP levels.

On it's efficacy from clinical trials
About 50% will have half their attacks go away
Correct (although 30% on placebo also have half their attacks - the effect of the drug therefore is 50% less the placebo effect = 20%......but sematics)

"A third will have 75% go away."
20% is more accurate with 8% on placebo having the same result.

"15-20% will have all their attacks go away"

Wow, just wow.

That is a gross over representation of the 100% responder rate.

I can't remember seeing a single trial for any CGRP meds that hit double figures for 100% response - most were in the 5% range with placebo commonly 2-3%.

This is one trial for Ajovy and two for Emgality, but the numbers are quite similar across CGRP mAb trials:
Silberstein, S.D., Cohen, J.M., Yang, R. et al. Treatment benefit among migraine patients taking fremanezumab: results from a post hoc responder analysis of two placebo-controlled trials. J Headache Pain 22, 2 (2021). https://doi.org/10.1186/s10194-020-01212-4

Skljarevski V, Matharu M, Millen BA, et al. Efficacy and safety of galcanezumab for the prevention of episodic migraine: results of the EVOLVE-2 phase 3 randomized controlled clinical trial. Cephalalgia. 2018;38:1442–54. https://doi.org/10.1177/0333102418779543.

Detke, H. C., Goadsby, P. J., Wang, S., Friedman, D. I., Selzler, K. J., & Aurora, S. K. (2018). Galcanezumab in chronic migraine. Neurology, 10.1212/WNL.0000000000006640. doi:10.1212/wnl.0000000000006640

Medications are a necessary means to get symptoms under control for many. Why the need to mythologise their impact?

Under experimental models CGRP released from the trigeminal ganglion is co released with substance P - yet this is not elevated in migraine studies.
Why?
CGRP is also expressed in the cervical dorsal horn where upper cervical nerves mix with trigeminal afferents.
Has this been excluded as a source?
Good scientific hypothesis testing would attempt to prove the null hypothesis - that is, prove yourself wrong and fail. Sadly, this fails to happen in many studies to develop medications.

Many questions remain to be answered about the actual role of CGRP in migraine. It is disappointing that the expert commentary diverges from factual discussions too often, and these 'hopes and opinions' are repeated often enough to become lore.

Interview Notes Study: “Ubrogepant for the treatment of migraine attacks during the prodrome: a phase 3, multicentre, randomised, double-blind, placebo-controlled, crossover trial in the USA” Article: “PACAP-Targeted Antibody Lu AG09222 Demonstrates Positive Results in Phase 2 Migraine Trial.....

05/03/2024

It's Cyclic Vomiting Syndrome Awareness Day 2024. Its a condition we see quite often, so we thought we'd put together a little video explaining what it is, and how we treat it.

21/01/2024

As a research active clinic, we always have some research projects on the go.

After the release earlier this year of our Vestibular Migraine Case Series (link in bio), we're working hard to publish on :
- Migraine with aura case series
- Chronic nausea and vomiting case study
- Persistent post-concussion syndrome study.

Contact us if you would like to know more about anything we're working on.

19/01/2024

We have been very busy on the research front with four projects all at various stages of completion.

Our case series, co-authored with Dean Watson, has recently been published and peer reviewed!

Our 3 participants had an amazing response to treatment. View the post for more details on the changes seen.

While we treat VM on a daily basis, research with large cohorts can be costly and time consuming, so chose to report on only 3 as we are primarily a private clinic treating patients, and any research is undertaken on a voluntary basis outside of usual work hours.

URL to the article (link in bio): https://healthopenresearch.org/articles/5-12/v3

08/01/2024

In person and telehealth Clinical Nutrition Consults now available at the Melbourne Headache Centre. Call us on 03 8648 6487 and ask to talk to Kristie to find out more.