Our journey into uncovering Fibromyalgia continues.
Previously, we introduced Fibromyalgia Syndrome (FMS) as the elusive, mysterious yet very common chronic pain condition, that has gone under or misdiagnosed for decades. In this previous Smart TMS post we discussed the key characteristics of FMS and what it means to live with the condition. Now, we delve into the inner brain mechanics of what makes FMS so troublesome.
Like a Sore Thumb
The reluctance to legitimise FMS as a real chronic pain disease is not solely down to a lack of research. In the past, we simply did not have the technical means to identify brain pain sensitivity in FMS patients. Developments in FMRI imaging can show us clearly that there is an unusually high neuropathic response to pain. Professor of Rheumatology, Daniel J. Clauw, conducted a study where they scanned the brains of FMS patients and healthy control participants. Both parties were painfully stimulated by pressing down on each participant’s thumbnail (very nippy, wouldn’t recommend). Brain activity was simultaneously monitored in an FMRI. Blood flow was observed in a variety of areas that play different roles in experiencing pain – from pain severity to our cognitive-emotional response to it.
The results found indicated a clear contrast between healthy participants and FMS patients. In FMS patients, the FMRI detected an enhanced response in regions responsible for processing pain; the somatosensory primary, secondary and association areas, in the insula, putamen and in the cerebellum (Gracely, Petzke Wolf & Clauw,2002). This is one of the few studies that show clear structural abnormalities in FMS brains – making the argument against the existence of FMS a bit trickier to refute.
An interesting comparison in pain perception was also made during this study. Of the 43 FMS participants that were painfully stimulated, they all reported the stimuli to be overall less unpleasant than the healthy participants. In other words, the FMS participants could manage the pain far better. This reduced emotional response to the pain suggests that FMS patients’ brains have adapted mechanisms where they are far more tolerant of moderate-to-strong pain. If you were to ask most people who have been living with FMS for a while, the likelihood is that they would agree they can become, somewhat, used to the daily pain.
Big Brains, Little Brains
Many areas of the brain allow us to process pain, some more than others. The Primary Somatosensory Cortex, or “S1”, has several functions. One of them includes being responsible for sensory discrimination, helping the rest of the brain determine where the pain is located. What do know about FMS? – It’s widespread pain. If you’ve already guessed that this means that S1 increases in size in chronic pain conditions, you’re correct. S1 is working overtime, trying to tell you where your pain is located throughout your body (Kim et al., 2015).
In reverse, decreases in brain structure size are closely linked to FMS. A meta-analysis of 13 studies evaluated brain activity during nociceptive (physical) pain stimulation. Again here, higher pain-processing activation was seen in comparison to healthy controls. The FMS brains were more active than normal when an incoming danger threat was detected. These studies concluded an overall decrease in functional connectivity, related to a decrease in grey matter. So, in short, the brain’s ability to process pain in a normal way has shrunk. Where there are problems, your brain will always try to outthink itself and come up with a solution. The decrease in size may be the brain’s way to try and minimise as much activity as possible, and to cope with this abnormality.
Hey! – Can you turn that down?
So, we can be pretty certain that the FMS brain processes pain differently and structurally changes in size to compensate for this. We have a good idea of what is happening neurologically, and there are innumerable other unmentioned biological components that are also involved. There are a lot of potential explanations as to why FMS pain occurs. Is this overwhelming? Perhaps. But fortunately, some explanations are more comprehensive and robust than others. Central sensitization leads to some answers.
Central sensitization is pain that originates from your brain, rather than physical or nerve pain. It is commonly discussed across many chronic pain conditions, in that it’s experienced throughout the body. Here, we can draw upon Daniel J. Clauw’s analogy of central sensitization and FMS like an electric guitar.
It can be easy to forget that pain is a useful biological response to help keep us safe, rather than a debilitating phenomenon, designed simply to make us suffer. Pain is inbuilt within us to tell us information about our environment, specifically – danger. The level of pain can tell us how threatening the environment is, by sending out “danger signals” at an appropriate rate. While a paper cut may sting, it won’t leave you writhing in pain for hours on end. The issue with central sensitization is that it amplifies pain.
Normal Pain Processing
Imagine that your body, with all the peripheral nerves and sensory neurons, is an electric guitar – practically the strings on the guitar. The adapter cable (your spine) sends the “danger signals” to your amplifier (your brain) and the sound produced represents how intense that pain is. The graphic above represents a pain processing system where the “volume” in the amplifier is at a neurotypical level. The paper cut is just that: a paper cut.
Central Sensitization / Abnormal Pain Processing
The graphic above highlights how central sensitization sets an abnormally high response to pain. The “volume” in the brain is too high. Even though the strings could be played lightly, the sound produced is still enhanced. Normal sensations throughout the body are perceived as dangerous and painful and are felt throughout the entire body. So, the paper cut may well feel like a gunshot wound to the hand. This analogy can help us understand why FMS suffers experience pain the way they do and why there are no psychical markers. The problem is not that their body cannot handle pain, their pain processing settings are too high!
Getting the Balance Right
There are some explanations as to what makes the volume setting so overly sensitive and unmanageable for the brain. Neurotransmitters, the chemical messengers in my brain, play a large role in pain processing. There are specific neurotransmitters that both help to facilitate “danger signals” that travel to the brain, and neurotransmitters that try and inhibit the impact of these signals. Think of it like two pathways that are working in tandem to modulate your pain experience (Littlejohn and Guymer, 2020).
The above diagram shows the direction of the neurotransmission abnormalities. Substance P is a moderator of pain, and increased levels have been associated with FMS (Yellin, 1996). Glutamate and Nerve Growth Factor (NGF) in high levels are also associated with increased pain. Others highlighted in the inhibition pathway, such as low levels of serotonin, norepinephrine, and dopamine has been considered one of the leading reasons for the increased “volume levels” in pain processing (Philips and Clauw, 2011). In short, the neurotransmitters are too active, which causes the brain to experience more pain than it should. The neurotransmitters that combat pain are then too low, and there are not enough of our bodies natural painkillers to soothe the suffering.
Much of FMS still remains unclear. Why is neurotransmission unbalanced? Put bluntly – we don’t really know. What triggers these brains’ maladaptive functioning to process pain normally? Let me get back to you on that one! And if all this evidence presented has left you thinking that there are lots of assumptions and fewer resolutions, you are in good company. Highlighting this evidence, however, is essential in breaking down the stigma and outright refusal to recognise FMS as a legitimate, chronic health condition.
But effective treatment exists! It can help make life with FMS not just bearable, but one worth living. In our third and final blog installment, we will introduce TMS as an effective method of managing Fibromyalgia.
Smart TMS Edibnburgh Practitioner
Gracely, R. H., Petzke, F., Wolf, J. M., & Clauw, D. J. (2002). Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis & Rheumatism, 46(5), 1333-1343.
Kim, J., Loggia, M. L., Cahalan, C. M., Harris, R. E., Beissner, F., Garcia, R. G., … & Napadow, V. (2015). The somatosensory link in fibromyalgia: functional connectivity of the primary somatosensory cortex is altered by sustained pain and is associated with clinical/autonomic dysfunction. Arthritis & rheumatology, 67(5), 1395-1405.
Littlejohn, G., & Guymer, E. (2020). Key milestones contributing to the understanding of the mechanisms underlying fibromyalgia. Biomedicines, 8(7), 223.
Phillips, K., & Clauw, D. J. (2011). Central pain mechanisms in chronic pain states–maybe it is all in their head. Best practice & research Clinical rheumatology, 25(2), 141-154.
Yellin, J. (1996). Why is substance P high in fibromyalgia?. Clinical Bulletin of Myofascial Therapy, 2(2-3), 23-30.