More than half (52%) of people will have a tension-type headache at some point in their life, around 18% will get a migraine, and 4% will suffer from chronic daily headaches. These are the most common headache-related diagnoses. Although there are some variations globally, the figures seem remarkably consistent across populations.
Secondary headaches can be initiated by triggering factors such as medication overuse, medication side effects, neck pain, sinus disease or dental problems. These account for small percentages individually compared to the primary headaches, but may be more treatable if the predisposing problem can be sorted out.
Tension-type headaches (TTH) feel like a dull or heavy, non-pulsating band of pain, usually on both sides of the head. The name comes from an erroneous belief that overly tight muscles are the main reason for the headache.
TTH usually occurs in episodes, with each lasting from several hours up to a few days at a time. There is not usually much associated nausea, light sensitivity or sound sensitivity.
Chronic TTH is a less common form and is diagnosed when you have experienced at least 180 days with a headache per year. It is generally not aggravated by routine physical activity; it’s just there all the time.
Genetic tendencies explain some of the risk for developing TTH, with your own risk increased threefold if you have an immediate family member with the condition.
Infrequent episodic TTH does not appear to be strongly associated with psychological stress, despite this common belief. Chronic TTH has a stronger association with higher psychological distress, but it is unclear whether this is a cause or effect of having long-term disabling headaches.
Strangely for such a common and problematic condition, there is still little agreement about exactly how the pain is produced in TTH.
The most attractive hypothesis to me is that it represents a “virtual” pain whereby multiple low-grade inputs (likely including inputs that are “almost-painful”, or below the threshold for conscious pain) add up to produce sensitisation of the trigeminal nerve nuclei (the nerve shown in orange below).
This turmoil registers as pain referred to the distribution of the head, usually the forehead, temple and back of the head locations. Examination of these areas doesn’t show any abnormalities because in TTH, there is no one driving mechanism of the headache.
Treatment remains almost trivially simple, despite years of research. It’s almost true to say that the proverbial “cup of tea, a Bex and a good lie down” sums it up. Aspirin, paracetamol or ibuprofen plus rest and possibly some cold packs seem to be the most reliable treatment. There is conflicting or negative evidence for almost every other, fancier therapy.
Migraine alone is the sixth most disabling condition globally.
Migraines are usually one-sided, associated with nausea and light sensitivity (photophobia) and may also be preceded by idiosyncratic sensory experiences called an “aura”. Aura phenomena can include moods or emotions, such as deja vu, visual symptoms (flashing lights or jagged lines are common) or problems with speech.
Migraine is a clinical diagnosis; there is no objective test that can verify it with our current technology. But compared to the frustration of researching and treating tension-type headaches, migraine has been steadily giving up its secrets over the past decade.
Migraine physiology is extremely complex. The headaches seem to arise because of dysfunctional regulation of the tone of some of the blood vessels inside the skull.
Migraine sufferers – Migraineurs – may have genetic vulnerability to migraines because of overly responsive calcium channels in their nerve membranes or other mutations which result in them having overactive signalling pathways in the brain.
Environmental or internal triggers can provoke these nerves to over-react, resulting in the activation of a reflex pathway. This dysregulation of normal structures causes the headache, nausea, photophobia and phonophobia (sound sensitivity) typical of an attack.
The period of headache in a migraine attack corresponds with a rise in the blood levels in the head of a peptide called calcitonin gene-related peptide (CGRP). CGRP is one of the most common pain-inducing signal molecules in the body. When the CGRP falls, the headache goes away. Where the extra CGRP comes from is not clear but it probably is released from the overactive networks of cells in the brainstem.
The most effective group of drugs for migraine are the triptans. So effective and specific are these drugs that the diagnosis of migraine needs to be reconsidered if they don’t abort the headache attacks most of the time.
Triptans work by activating certain subtypes of serotonin receptors in the brain. Taking a triptan early in a migraine attack seems to directly lower the CGRP release and oppose its effects on blood vessels thereby stopping the attack. Triptans are not however useful to prevent frequent attacks of migraine.
Migraine prophylaxis is achieved by several drugs of different classes, with radically differing mechanisms of action. Some are anticonvulsants, which clearly work by suppressing the nerve overactivity typical of migraineurs. Others, such as the beta-blockers (propranolol) and calcium-channel blockers (verapamil) target the nerve endings on the blood vessels. Others which are known to be effective, such as botulinum toxin (Botox) and amitriptyline (Endep) work by means which are yet to be fully understood.
Severe migraineurs suffer years of disability and as a public service I would like to suggest that if you know someone who has severe migraines (you almost certainly do) please read this excellent list of what not to say to them when trying to be sympathetic or helpful.
Chronic daily headache
Imagine that you never had a day without headache. You can remember vaguely the time when you didn’t feel that pounding in the temples, squeezing in the back of the head or piercing pain above the eyes but it seems like another life. Such is the lot of sufferers of chronic daily headache (CDH).
Some headaches begin as as frequent but clearly episodic tension-type headache, or migraine, but then “transform” into what seems to be basically a continuous headache for at least some part of every day.
There are a number of rare headache types which may cause chronic daily headache and diagnosis of the these can lead to specific treatments which work well. This is the role of a neurologist or pain specialist with a special interest in headache.
Possibly the most common reason why tension-type headache or migraine can transform is medication overuse, especially short-acting opioids such as codeine. The best solution to this problem is to avoid long-term regular use of codeine for headaches, though the evidence would suggest we may never achieve this goal except by making codeine prescription-only.
Frequent use of triptans is also believed to sensitise the trigeminovascular networks in the brainstem, thereby lowering the bar for triggering of migraine attacks. If the threshold for an attack becomes too low, they may never quite switch off, and one attack will run into the next one.
If you have more than just the occasional headache, it pays to get a proper diagnosis, as the reasons for your headache can be many and varied. Some have specific treatments for them, and others such as TTH seem quite difficult to find a specific treatment for. There are new classes of drug treatment under development, for migraine in particular, so it looks hopeful that future generations may not have to labour under the burden of poorly treated headaches.