Blood pressure and headaches, Part 2

In our last article, we presented several explanatory approaches to the connection between blood pressure and headaches. In this continuation, we will be explaining a further, much-discussed scientific finding and will be taking a look at the future of research.

High blood pressure – Hypalgesia – Headaches: only an apparent contradiction?

One theory has been discussed in the scientific community for a long time: the theory of so-called hypalgesia with hypertensives. It states that the general sensitivity to pain is reduced for patients with high blood pressure. This phenomenon was first described in 1980, and subsequently confirmed through further studies. This solidified an assumption that had already been set out in a New York study in 1913, according to which people with high blood pressure fundamentally have a higher pain perception threshold. With regard to the comorbidity of headaches and high blood pressure, the following question arises: if people with high blood pressure do not sense pain as quickly as people whose blood pressure falls within the normal range, how is it then possible that hypertensives experience headaches more frequently than people without high blood pressure?

What was evolution thinking? A possible reason for hypertension and hypalgesia

There has not yet been any clarification on the mechanisms underlying the reduced pain sensitivity of high blood pressure patients. It seems certain that the body’s so-called baroreceptor system plays a role. It is responsible for the perception and adjustment of blood pressure, through different neuronal mechanisms (so-called endorphinergic and noradrenergic central neurons). In addition to their pressure-regulating function, these also have connections to our pain perception system and – as an extensive review has already presented in 1996 – to further central control processes, which contribute to the processing of stress, aggression, readiness to escape, or also relaxation, among other things. The author of the review also refers to a “reward system” in connection with reduced pain perception, which is always activated when the organism is exposed to stress – which, physiologically, can be accompanied in many situations by an increase in blood pressure. This could also explain the possible evolutionary reason for these parallel processes: when an organism is under stress, blood pressure could be increased with the aim of achieving a better fight and flight readiness; in turn, pain perception should be minimised as far as possible for this reason, so that the organism is not “unnecessarily” held up or paralysed by pain, but is maximally responsive. Thus, phasic blood pressure increases could constitute an adaptive stress response, through the inverse relationship of blood pressure and pain.

The wide field of blood pressure occurrences

Therefore, pain perception seems to be only one of many aspects which are connected to current or even chronic blood pressure occurrences. Presumably, it must generally be placed in a broad context with the mechanisms which are responsible for maintaining homeostasis (balance in the organism). This could also explain how studies sometimes have contradictory or even barely interpretable results. Furthermore, it must be noted that the hypalgesia theory pertains to general pain perception. Many studies on this topic were specifically researched on pain conditions which are not headaches – for example, on chronic back pain or pain through heat irritation. Whether and to what extent the obtained results are applicable to other or all types of pain, and therefore also generally to headaches and specifically to different types of headaches, has not yet been answered.

What we still want to know

With regard to the simultaneous occurrence of high blood pressure (with assumed hypalgesia) and, generally, headaches and, more specifically, migraines, the following possible research questions are opened up:

• In high blood pressure patients with a predisposition to migraine, do the trigger factors in certain situations prevail in their effect against an existing hypalgesia, which is why a migraine headache develops despite the fundamentally reduced sensitivity to pain?
• Can it be assumed that the headache which is actually felt would be even more severe without the conditions brought about by an existing hypalgesia, than was actually perceived by the affected people?
• Is migraine, as an independent neurological illness, fundamentally subject to rules which cannot be controlled or can only be controlled insufficiently though homeostasis regulation?
• Do headaches generally occur when the body’s regulatory mechanisms are working to the limit, or their effectiveness is impaired by other factors – which is why the effects of regulation are of little to no importance for the development or perception of headaches?

Despite or precisely because of the continued great need for research in this area, the current advice for everyone suffering from headaches or migraine is still to become familiar with your own pain as much as possible. If you know your personal trigger factors and learn to integrate headache prevention behaviour into your daily life as effectively and sustainably as possible, you can automatically intervene in your own headache situation and carry out prevention in the best sense, independently of the processes currently taking place in homeostasis.