​Why is that that the same thing can be a trigger and a treatment? Headache sufferers have had a love-hate relationship with caffeine, going from complete avoidance due to its triggering potential, to relying on a cup a day to keep pain at bay!
 
Hidden amongst our morning tea and coffee, soft drinks and chocolate is a potent drug that has very complex interactions that go right to the heart of headache and migraine.

​Caffeine is a chemical compound in the alkaloid family, (chemical name 1,3,7-Trimethylpurine-2,6-dione) that occurs naturally in over 60 plant species including tea, kola nuts, coffee beans, mate leaves, guarana plants, and cocoa nuts. As such caffeine is one of the most widely consumed psychoactive agents (able to change brain function/mental state) in the world. [1]

​When entering the body caffeine looks exactly the same to nerve cells as a substance called adenosine. Adenosine is active in a number of regions in the brain and is a key building block in our energy pathways, but doesn’t instantly boost energy. In fact adenosine binding to nerves in the brain causes drowsiness by slowing down nerve activity and promotes sleep. During this time our blood vessels dilate allowing more blood into the brain to nourish it during sleep.
Caffeine blocks the ‘drowsiness effect’ by binding to adenosine receptors, leading to increased nerve activity and an increase in our ‘alertness’.
In response to this increased activity the pituitary gland releases adrenaline – our fight or flight hormone. The result is what most people will feel when they drink coffee in increased activity of the central nervous system: increased heart and breathing rate, increased blood pressure, increased diuresis, cardiac muscle contraction and gastric, lacrimal (tear), nasal mucous secretions vasoconstriction of blood vessels in the brain. Blood will be moved from your periphery to your core and the liver will release more glycogen into the blood stream for extra energy.

​Caffeine causes vasoconstriction in the brain, and was added to numerous migraine medications on the mistaken assumption that migraine was a vascular headache.
‘Now that migraine is thought to be a neurological and not a vascular disorder, caffeine’s common inclusion in migraine treatments suggests an alternative, non-vascular mechanism of action behind its efficacy in migraine patients.’(Nathan Fried 2017)
While there may be some mild benefits with the vasoactive effects of caffeine, it is caffeine’s action in blocking adenosine receptors in the brainstem that is having the positive impact. In the brainstem (the home of the migraine circuit) adenosine is involved in pain transmission and sensitization. By blocking adenosine receptors here caffeine may help stop the spread of ‘excitability’ and abort a migraine or ease a headache. [2] 
 
Despite the anecdotal evidence or a ‘strong black coffee’ aborting migraines, research into caffeine as a monotherapy (not combined with another drug) shows it is no more effective than placebo in time taken to 50% reduction in symptoms. [3]
 
The most commonly understood mechanism for helping headache and migraine sufferers comes from caffeine’s effect on your stomach. Ingesting Caffeine causes rapid lowering of gastric pH (more acidic), improving the absorption of analgesic medication. When the ergot family of drugs was in use a combination therapy known as cafergot was widely used. This has since been removed in most forms (still available as a suppository under prescription), due to deleterious cardiovascular effects of ergotamines. Today we see panadol extra on the market with caffeine combined with paracetamol. Despite some research to support its use as a combined therapy there isn’t currently a caffeine plus NSAID (like ibuprofen) on the market. This will be because both agents cause lowering of gastric pH, which indeed is the most common and concerning side effect of NSAID’s leading to stomach upset and ulcers.
 
Once again we see the double-edged nature of caffeine. On the one hand, here there seems to be good reason to use it as either an adjuvant to other rescue medication, or for its own effects in dampening brainstem excitability, however there is evidence to the contrary. Not unlike the opioids (with similar dependence and withdrawal profiles) caffeine may seem to ne helping with one hand, but worsening things in the long run.

​A study of 36 children and adolescents (aged 6-18) who were heavy cola drinkers (minimum 1.5L per day or 192gms caffeine) and suffered daily headache examined the effect of ceasing caffeine consumption. Two weeks after stopping their caffeine intake researchers saw a complete cessation of daily headache in 33 of the 36 children in the study. [4]
 
 
Another study examining the factors that lead to chronification of headaches found daily consumption of caffeine to be a significant factor in the development of analgesic overuse headache and chronic migraine. [5]
This study was followed up 2 years later looking more closely at the amount of caffeine used, and found a history of heavy caffeine use (> 300mg daily) was associated with chronic daily headache compared to episodic headache control groups. [6]
 
In 2016 Lee and associates looked at the effect of caffeine cessation on the effectiveness of acute migraine medication. The two groups (abstinence and coffee groups) had a mean caffeine intake of 192mg per day. Given it’s adjuvant effect with analgesics one might assume that cessation of caffeine use would decrease the effectiveness of acute migraine treatment. In fact they found the exact opposite. Discontinuing caffeine use actually significantly improved the efficacy of acute migraine medication. [7]

​There appears to be a complex association of caffeine with headaches. On the one hand many properties seem to make it a useful medication for helping relieve pain, but daily use appears to have some negative effects in increasing the likelihood on transforming from episodic to chronic headaches. 
 
It’s the same story we have been hearing for opioid analgesics like codeine, recently taken off the shelves as an OTC (over the counter) medication. Adenosine homeostasis also plays a crucial role in narcotic drug responses and plays a role in neurobehavioural features associated with opiate addiction and withdrawal. [8]
Caffeine also affects dopamine by increasing its production in the brain. Dopamine is our ‘pleasure drug’ so it makes you feel euphoric. This action is very similar to two banned drugs in heroin and cocaine which both slow down dopamine reabsorption. It’s the action on dopamine that may be even stronger cause of addiction and withdrawal with caffeine.
In other words the effect of caffeine and its interaction with adenosine and dopamine receptors results in the same withdrawal/addiction responses in our central nervous system as narcotic drugs.

​The Food Standards Code (Australian government) restricts the caffeine content of energy drinks. Whilst they have not set an upper limit in Australia, they have commented on the limit that appears to be linked to anxiety as being 3mg of caffeine per kg of body weight. This equates to around 200mg per day for an adult, and that seems to be a similar figure in the headache studies above. [9]
 
At the end of all this you firstly need to figure out whether caffeine has any interaction with your headaches at all, as triggers are a hugely individual aspect of headaches.
 
If you believe caffeine is a sensitive trigger with either not enough or too much (i.e. you have a ‘sweet spot’ in terms of it being helpful), you may want to monitor how much you have on a longer-term basis. 200mg per day, whilst in the short term may seem like its helping, in the longer term may actually be making you worse.
 
An espresso shot may contain anywhere from 30mg to 90mg per shot. This variation is in the bean and roast type with lighter roasts having more caffeine. Caffeine in other foods drinks as per Food Standards Code [9]:
Black tea – 20-80mg/250ml (longer brewed = higher caffeine)
Coca Cola – 48.75 mg per 375ml
Milk Chocolate – 20mg /100g
Dark Chocolate – 81mg/100g
Energy drinks – 80mg/250ml
 
So one double shot of light roasted barista espresso coffee could have you close to the 200mg level. In the USA the recommended daily intake for caffeine is 400mg. The discussion around triggers always comes back to dealing with the common underlying theme which is an overactive brainstem. Lots of people consume caffeine but don’t get headaches, even when they stop or withdraw.
 
So what makes headache and migraine sufferers prone to the positive and negative impacts of caffeine. Indeed why do all these different triggers result in headache? The underlying problem is overactivity in the brainstem – in the area housing the nerves for the head/face and neck.
 
Regardless of the impact of triggers, the neck is the most common source of overactivity in this part of the brainstem and is the easiest to assess and treat.
 
Treat the underlying causes today and get your neck assessed.

 [1] Neurology advisor Caffeine-migraine-headache-trigger-treatment
 
[2] Fried, N.T, Elliot, M. B. and Oshinsky (2017) The Role of Adenosine The Role of Adenosine Signaling in Headache: A Review. Brain Sciences, 7 (3), 30.
 
[3]Diener HC, et al. The fixed combination of acetylsalicylic acid, paracetamol and caffeine is more effective than single substances and dual combination for the treatment of headache: a multicentre, randomized, double-blind, single-dose, placebo-controlled parallel group study. Cephalalgia. 2005;
 
[4] Hering-Hanit R, Gadoth N (2003) Caffeine-induced Caffeine-induced headache in children and adolescents.Cephalalgia, 23, 332-335.
 
[5] Bigal, M.E. Sheftell, F.D, Rapoport, A.M., Tepper, S.J. and Lipton, R.B. (2002) ChronicChronic daily headache: identification of factors associated with induction and transformation.Headache, 42 (7), 575-581.
 
[6] Scher, A.I., Stewart, W.F, and Lipton, R. B. (2004) Caffeine as a risk factor for chronic daily headache: a population based studyNeurology, 14; 63 (11) 20022-7.
 
[7] Lee, M.J., Choi, H.A., Choi, H, and Chung, C.S. (2016) Caffeine discontinuation improves acute migraine treatment: a prospective clinic-based study.Journal of Headache and Pain; 17 (1); 71 
[8] Mohong, Wu et al (2013) Opiate-induced Changes in Brain Adenosine Levels and Narcotic Drug Responses. Neuroscience, 3, 228; 235-242. 
[9] Food Standards Code (2018) Caffeine
 
[10] Heckman et al (2010) Caffeine (1, 3, 7-trimethylxanthine) in Foods: A comprehensive Review on Consumption, Functionality, Safety and Regulatory MattersJournal of Food Science, 75, (3).
 

Reason 5 - Our guarantee.

We have heard this story so often it makes me feel a little ill. I have been seeing my (insert one of chiro, physio, osteo, masseur, etc) once a week for 6 months - and it seems to help for a day or so.

This is not helping. It is treating the symptoms, and because it is not getting at the underlying cause it is ultimately ineffective, expensive, and treatment without an endpoint.

Our guarantee has 2 parts. The aim is to minimise the risk of treating people who either don't have a neck problem relating to their head pain, or not continuing to treat people who are getting no more than short term relief.

Firstly we don't book everyone that calls for an appointment. We conduct a phone interview lasting approximately 10-15 minutes seeking information that may save you the time and money of an initial consult. Some people from the phone interview will be referred back to their GP or specialist for further investigation or referred back to their local health professional (Physio/Chiro/Osteo) for follow up.

Those that are accepted will then book an initial assessment. Here we look for clear signs that your neck is related to your condition. By very selectively and precisely stressing the joints in the top of the neck we look to temporarily reproduce the area of your usual symptoms (i.e. push pain up into your head behind the eye). If we can reproduce these symptoms we sustain the pressure and look for the referred pain to ease after 30-40 seconds. 
If this "reproduction and resolution" of familiar symptoms occurs (and it does in approx. 80% of initial assessments) we accept the person into the initial treatment block.
If we cannot reproduce familiar symptoms, or we can but they do not subside then it is unlikely the treatment we use will be effective, so rather than try and convince you to get a treatment that will ultimately provide short term or no relief and little else, we set ourselves apart from the crowd and decide not to treat you.

Secondly, if you are accepted into the initial treatment block, then we expect there to be significant changes in your condition within 2-3 weeks. That is not to say that you will be "cured" in 2 weeks. If we get to the end of the second treatment week after the initial assessment, and there is no sign of significant change we stop.This is a protection for the 10% of cases who start treatment, and their condition does not respond preventing the cycle described above of "endless" treatment programs with no goals. This number is relatively low, indicating over 90% of people respond. The reason for such a high success rate is due in part to screening out 20% from the initial assessment, but unfortunately there are some whose necks will not respond to treatment in the long term - we will not continue to treat if you are not improving.

We would love to be able to help everyone, and we would love everyone to respond well to treatment. The reality is that only 80% have treatable problems related to their neck, and approximately 90% of these will respond to treatment. The difference is we are upfront about these numbers, and open about every step of the process to minimise the risk of receiving treatment that is ultimately not effective.

The improvement in the first few weeks is why this clinic can effectively run outreach services to regional areas. Those that do respond, respond quickly and are able to manage with self treatment soon thereafter.

In part 1 we explained the underlying cause of menstrual migraine, as it is with other chronic headache and migraine types, is an overactive part of the brainstem called the trigemino-cervical nucleus or TCN. At the heart of this over activity is the interconnection in the TCN between the nerves from the upper part of the neck, and the nerves thatsupply the head and face. Hormones simply make it easier for this overactive brainstem to cause migraines. Let me explain further.

Oestrogen plays a critical role in the production of serotonin and also helps the brainstem to absorb serotonin. When oestrogen levels drop around day 1 of the menstrual cycle the levels of serotonin drop as well. 
Changes in the level of serotonin have a significant impact on headache and migraine. In fact the medications from the triptan family (e.g. Imigran, Naramig, Maxalt, Relpax, Sandomigran) are effective because they make the brainstem absorb more serotonin. 

So what does serotonin do?
Increasing the levels of serotonin decreases activity in the brainstem, and stops activity “spreading” to the extent where it “switches on” the nerves of the head and face causing pain – a headache or migraine. It’s not just having more serotonin though. Too much as well as not enough will cause problems because serotonin also impacts on the blood vessels on the lining of the brain.
A decrease in Serotonin will cause these blood vessels to dilate, contributing further “information” to an already overactive brainstem. Added to the loss of control of this over activity and it is not hard to see why the nerves in the head are “lit up” causing a migraine.

Around mid cycle when oestrogen levels rise, serotonin levels rise causing blood vessels to constrict. This mechanical input from constricting vessels is enough in some people to trigger another headache, similar to the day 1 migraine, but commonly far less intense and often not migrainous in nature. 

The fluctuation in oestrogen and hence, serotonin is no different in menstrual migraine sufferers and non-sufferers. This has prompted leading expert in menstrual migraine Elizabeth Loder to say: 
“We must look at other factors (other than hormones)…………. Abnormal central nervous system response to normal fluctuations in hormones is the likely underlying cause of menstrual migraine”. (2001)

Menstrual migraine is treatable, not by trying to treat hormones, but trying to treat the underlying activity in the brainstem. The upper cervical spine has the most significant input into the brainstem and in 80% of cases the usual pain of migraine and headache is able to be “switched on” by selective and specific pressure applied to the upper part of the neck. If this reproduced pain eases as we sustain the pressure, then treatment will be successful in 90% of cases.

The brainstem of chronic headache and migraine sufferers is overactive.

Insights 1 and 2 examined the anatomy of headaches – the trigeminal nerve intermingling with the upper cervical nerves in the brainstem. The scientific evidence for the abnormal physiology (overactivity) involved in all major headache types is clear.

With an unknown aetiology (cause), headaches were historically described according to symptoms. This view persists today with the International Headache Society’s  (IHS) current classification system (1). This led to treatments targeting symptoms, and caused researchers and clinicians to speculate about the underlying cause.

Migraine’s typical throbbing pain was assumed to be due to blood vessels constricting and then dilating. This theory gained much support and is still cited by many today, however research in the past two decades has disproven it prompting the president of the IHS to write “The vascular theory of migraine – a great story wrecked by the facts” (2).

The “tightening” quality of tension headache was thought to be increased scalp muscle tension. In 1977 an EMG study (measures muscle activity) showed that the tension of scalp muscles was no different to non-headache sufferers, yet the muscles in the top of the cervical spine significantly increase activity (3).

The two widely accepted theories regarding the underlying aetiology of headache and migraine were effectively dead.

So what then is the underlying problem and how do we know?

Three key areas of research combine to tell the story of an overactive brainstem.

Positron emission tomography (PET) scans show activity in a part of the body. The trigemino-cervical nucleus (TCN) has been shown to have increased activity using PET scans (3-4). This overactivity is present during and after the attack indicating it is not as a result of the attack, but constantly present and fundamentally contributing to the attack.

The triptans (e.g. Imigran, sumatriptan, Zomig, Maxalt) have a strong effect on a form of Serotonin highly specific to the TCN, which as previously described, has a dampening effect on activity in the brainstem and blocks pain signals from going up to the brain (6). Interestingly though, the triptans have demonstrated an effect in migraine, menstrual migraine, tension type headache, cluster headache and cervicogenic headache (7-10). This indicates all of these headache types have a common underlying problem - overactivity of the TCN.

Reflexes provide information about activity in the central nervous system (CNS). If a reflex is weak or absent, it is indicative of decreased CNS activity. If a reflex is heightened it is indicative of an overactive CNS. There are two reflexes (nociceptive blink reflex and trigeminocervical reflex) that relate directly to the TCN in the brainstem.

Both of these reflexes are overactive in migraine, menstrual migraine, tension type headache, and cluster headache (11-14).

Remember from insights 1 and 2 all the areas the TCN relays information to the brain from. An overactive TCN could cause you to feel throbbing or tightening pains, get blocked ears, or pain in the teeth or sinuses, when in fact it is just the brainstem fooling the brain. The blood vessels, muscles and ears are fine as demonstrated in earlier studies.

The evidence is clear. Increased TCN activity is a central part of the headache and migraine story. The current dispute in the neurological community is about “what causes this overactivity?”

In the final part of the insights series (part 4) we examine the key area that can cause the brainstem to be overactive, and it is an area that has been largely ignored in headache and migraine - the upper cervical spine.

(1) IHS Classification ICHD-II. International Headache Society. http://ihs-classification.org/en/ Accessed 3/2/13.

(2) Goadsby, P (2009) The vascular theory of migraine – a great story wrecked by the facts. Scientific Commentary. Brain: A Journal of Neurology, 132; pp. 6-7.

 (3) Bakal, D.A. and Kaganov J.A. (1977) Muscle contraction and migraine headache: psychophysiologic comparison. Headache 17; pp. 208-15.

(4) Weiller, C. et al (1995) Brain stem activation in spontaneous human migraine attacks. Nature Medicine, July; 1 (7); pp 658-660.

(5) Afridi et al (2005) A positron emission tomographic study in spontaneous migraine. Archives of Neurology, 62 (8); pp 1270-1275.

(6) Goadsbay, P.J. and Hoskin, K.L. (1998) Serotonin inhibits trigeminal nucleus activity evoked by craniovascular stimulation through a 5HT1B/1D receptor: a central action in migraine? Annals of Neurology, 43 (6), pp 711-718.

(7) Ekbom, K. and Hardebo, J.E. (2002) Cluster headache: aetiology, diagnosis and management. Drugs, 62 (1), 61-9.

(8) Siow, H.C. et al (2004) Frovatriptan for the treatment of cluster headaches. Cephalalgia, Dec, 24 (12), pp. 1045-8

(9) Cady, R.K. et al (1997) Responsiveness of non-IHS migraine and tension-type headache to sumaptriptan. Cephalalgia, Aug, 17 (5), pp 588-90.

(10) Pavese N, Bibbiani F, Nuti A, Bonuccelli U. (1994) Sumatriptan in cervicogenic headache. Proceedings European Headache Federation 2nd International Conference; Abstract 131

(11) Nardone et al (2008) Trigemino-Cervical Reflex Abnormalities in Patients With Migraine and Cluster Headache. Headache, 48; pp 578-585.

(12) Nardone, R. and Tezzon, F. (2003) The trigemino-cervical reflex in tension-type headache. European Journal of Neurology, 10 (3), pp 307-312.

The anatomical pathway described in parts 1, 2 and 3 of this series have been known and recorded for several decades. To attribute credit to a single source for the information provided would do a disservice to some that have contributed to my knowledge over the years. Suffice to say that Professor Nikolai Bogduk from the University of Newcastle has produced a body of work over 30 years, which has greatly expanded our knowledge in this area and those that have taught me have undoubtedly drawn upon his publications.

(13) Gantenbein, A.R. and Sandor, P.S. (2006) Physiological parameters as biomarkers of migraine. Headache, 48 (7); pp 1069-74.

(14) Varlibas, A. and Erdemoglu, A.K. (2009) Altered trigeminal system excitability in menstrual migraine patients. Journal of Headache and Pain, 10; pp 277-282.

In part 1 we looked at the trigeminal nerve (cranial nerve V) as being the key nerve relating to headaches and migraine. This week we will look at where this information goes and how it is controlled.

Walking along a path you misjudge ducking under a tree and a low hanging branch scratches you on the forehead. Branches of the trigeminal nerve sensing pressure and movement under the skin are the quickest to react – sending information into your brainstem. Here the peripheral nerve ends, and passes its information onto a number of central nerves by releasing chemicals (neurotransmitter) across a small gap between nerves called a synapse. This meeting of the peripheral nerve with central nerves happens in a nucleus. The trigeminal nerve shares its nucleus with the upper three nerves from the cervical spine and as such the area is referred to as the trigemino-cervical nucleus (TCN). On top of that three other cranial nerves send pain input from all muscles of the face and scalp (via the facial nerve), the sensory fibres from the middle ear (via the Glossopharyngeal nerve) and sensation from the outer ear and the dural lining of the brain (via vagus nerve). This means that this little area in the brainstem is responsible for relaying all of the sensory information from the face, head and neck into the brain.

Back to our scratched head; some of the central nerves activated will cause an immediate response via a reflex loop - it happens without your control or without having to think. This may cause your eye to close (nociceptive blink reflex) and your head to turn away (trigemino-cervical reflex) to help protect you from further damage.

A spilt second later the information travels along another central nerve that relays that information to the brain. You now become “aware” that something has struck you. Another fraction of a second later the feeling of pain is registered (it travels along slower nerves) You then make an appropriate response that is mediated through the peripheral nerves i.e. look for the object that struck you, reach up to check your wound.

Nerve impulses arriving in the trigemino-cervical nucleus have multiple interconnections that can activate many different parts of the brain including memory and emotion. Lets illustrate the interconnections in the brain with another example. While sitting outside a plant’s branch is only just touching your ear. Your first reaction may be to swipe it away. Those with particular phobias may leap from their chair, maybe even screaming out, brushing anxiously at their ear thinking a spider is crawling on them.

No pain, and no “real” threat, but sensory information from the head and neck is treated differently (due to the importance of the brain and brainstem), and is often interpreted through memories and emotions, so our reaction to very minor sensations or “inputs” can be quite extreme.

We need to be able to control the “volume” of noise that the nerves are making. Most information coming into the TCN does not normally need to be “sensed” as a threat, and in fact is often not sensed at all. Information about movement from the muscles and joints in the neck, air movement from breathing, or touch sensation from the tongue moving in the mouth is not something that we need to be aware of. The brain has the ability to control the volume on information it receives, much like when you put on a woolen jumper – prickly for 30 seconds or so then you don’t notice it. It is no less prickly but your brain has turned down the volume.

“Volume” control in the brainstem is achieved using a neurotransmitter, or a chemical, much the same as we described above with the nerves forming a chemical junction or synapse. These neurotransmitters either excite (turn up) or depress (turn down) the activity of the nerves. We have different neurotransmitters controlling different areas so we don’t depress all nerves in all areas. The activity in the trigeminal nucleus is regulated by a neurotransmitter called serotonin. In fact serotonin has a significant role throughout the brain in areas related to mood, sleep, appetite, and has been associated with illnesses such as depression.

Put simply, Serotonin’s role in the brainstem is to set the threshold for pain. Any stimulus that goes above the set threshold will trigger a pain response in the trigeminal system – a headache.

There is very good evidence from multiple sources – reflex studies, PET scan studies (looking at activity of nerves) and from pharmacological studies (the Triptan group of drugs) that the Trigemino-cervical nucleus is “Headache” or “Migraine” central and is overactive.

In the next installment of “insights” I will outline what the abnormal trigeminal system looks like and why it has caused a major rethink in terms of the possible pain generators in headache and migraine.

For those that have read this far……you are truly dedicated and most likely you are a sufferer looking for an answer. I have a special offer for 5 people only (first in first served). The first to:

-      share this post

-       Go to the following page and redeem your offer as a thank you for your support:

http://www.melbourneheadachecentre.com.au/facebook-special-offer.html

Insights The Anatomy of Headaches - Part 1

Apologies for the many of you who have already read this - just skip past it. I've had some issues with Facebook, who turned my original post into a photo, which are now rectified. Please - like and share as you never know who you may be helping. Part 2 coming this weekend.

Headache and particularly migraine has developed an almost mystical quality within societies understanding. We have seemingly advanced so far in our knowledge of the human body, yet in this area, little in the public realm other than the development of new medications has changed in decades. In many circles the underlying pathology of headache is still treated as "unknown". Yet so much is known but unfortunately has not entered the public domain. I hope to change that for you in some way.

For us to sense pain anywhere, or indeed "sense" anything, nerves must be activated. The key nerve that informs our brain about what is happening in a vast majority of the head and face is the Trigeminal nerve - cranial nerve V.
This nerve, as indicated by its name, has three main branches; the opthalmic, maxillary, and mandibular nerves. From all the subdivisions of these three branches the nerve carries information back to the brain from the skin of the face and front half of the scalp (back of scalp and neck is upper cervical nerves), conjunctiva, mucous membranes of the mouth, nose and sinuses, the cornea, teeth, gums, palate, pharynx, tongue (except taste - i.e. position for speaking, pain/temperature, pressure), sensory information from the muscles in the face, temporomandibular joint (jaw), and out part of the tympanic membrane (ear drum).
Importantly it also has sensory receptors in the dura mater including blood vessels. The Trigeminal nerve has a small supply to muscles that are involved in mastication (biting, chewing) and swallowing and the ear drum.

See this diagram - courtesy of Gray's Anatomy.

Essentially, if you have a headache whichever type it is classified as, it is the Trigeminal system that is active, or over active as the case may be.

All the information from the Trigeminal nerve make their way into the skull and 'terminate' in the brainstem in an area called the Trigemino-cervical nucleus caudalis. Here the peripheral nerves of the Trigeminal system that we have just described above form a junction or synapse with the central nerves that then relay this information up to our brain.

It is in the brianstem, and particularly the Trigemino-cervical nucleus where the headache story really begins to unfold.

In part 2 of "Anatomy of a Headache" we will look at the Trigemino-cervical nucleus in more detail and see why there is so much interest in the upper cervical spine as a potential pain generator in headache and migraine.