Rare individuals born without pain perception (congenital insensitivity to pain, CIP) rapidly accumulate disabilities and tend to die young. Pain makes us withdraw from and subsequently avoid injurious situations, it prompts us to protect damaged structures such as eyes or joints, and it alerts us to diseases such as appendicitis that may prove fatal without treatment. And what is true of physical pain also applies to its emotional counterpart. Pain is good for us. It helps us to survive.
But what if pain perception goes haywire? Like all UK general practitioners, I have several patients with a frustrating if fascinating condition called fibromyalgia. Jane (as I’ll call her) is typical of the severe end of the spectrum: she’s a woman in her 40s (early middle-aged women are most frequently affected), her life is blighted by unremitting pain in muscles throughout her body and no painkiller gives her any relief (she has tried them all, even morphine).
Over the years she’s become progressively disabled, finding it harder to do even simple things such as help her young children dress, and she’s able to work fewer and fewer hours. Around 18 months ago she went long-term sick and earlier this year her employer terminated her contract. She’s now struggling to adjust to a life on benefits. Apart from the constant pain, one of the things she worries about most is other people’s disbelief. To casual observation, Jane appears in the pink of health.
People with fibromyalgia have precious little to show for their suffering. They have no swelling, inflammation, limp or deformity. Blood tests, X-rays, scans and biopsies are normal. Theirs is a subjective illness. They find that family and friends eventually tire of hearing about their intractable pain and its impacts. Little wonder that depression and anxiety are common complications.
To cap it all, their doctors frequently grow frustrated as they return, time and again, to report a distinct lack of improvement with each and every treatment they try. Over the years, many physicians have questioned fibromyalgia’s validity as a disease; physical symptoms are dismissed as “all in the mind”, the implication being that, in an unconscious way, these patients “need” their illness as a passport to duck out from the stresses, strains and dissatisfactions of everyday life.
Advances in imaging the functioning nervous system are beginning to shed light on what’s really going on. To experience pain, you have to have the requisite sensory apparatus: receptors (nociceptors) that detect harmful changes within the body’s tissues and organs; and nerve cells (neurons) that relay this information to the brain.
This sensory apparatus is missing in those rare individuals with CIP. But sensing alone is not enough. Once pain nerve signals reach the brain they are subject to what is termed central processing, involving a number of the brain’s most evolutionarily primitive regions, regions that are involved with raw emotional response – with fight, flight and survival. It’s this central processing that transforms nociceptor sensory input into our subjective experience of pain.
There’s a heck of a lot of other nerve traffic passing from body to brain that’s got nothing to do with pain. For example, our muscles are constantly generating information about their position, stretch and contraction, all of which ensures the apparently effortless coordination of our movements and balance.
In fibromyalgia, some of this non-pain information seems to become capable of triggering the brain’s central pain processing regions. The very fact of having normally functioning muscles begins to be experienced as chronic, widespread pain.
It’s not fully clear what causes this malfunction, but a process called central sensitisation is at its heart. We know that 30 per cent of patients with uncontrolled rheumatoid arthritis –where diseased joints constantly bombard the brain with nociceptive input – will eventually develop superimposed fibromyalgia. Sheer volume of pain traffic in the nervous system may be one factor in central sensitisation.
However, many fibromyalgia sufferers don’t have painful arthritis. Their fibromyalgia may be linked to genetically disposed abnormalities in brain chemistry. The chemicals (neurotransmitters) involved in central pain processing have different functions elsewhere in the nervous system, which may account for the additional symptoms many fibromyalgia patients experience – sleep disturbance, profound fatigue, and impaired concentration and thinking (“fibrofog”).
It’s as yet unclear what causes these neurotransmitter abnormalities to be “unmasked” at a certain time but intriguing studies into “pain memory” suggest that stresses in adult life may reignite central sensitisation originally developed in the context of severe emotional or physical pain when young, something that may explain the association between fibromyalgia and childhood abuse or trauma.
We’re still a long way from understanding fibromyalgia, but we are at least now aware that, as an illness, it’s all in the brain, if not the mind.