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  1. Politics
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21 November 2013

Pain helps us to survive – but it can also turn our own body into an enemy

When a patient is diagnosed with fibromyalgia, all too often symptoms are dismissed as "all in the mind".

By Phil Whitaker

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.

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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.

  1. Politics
  2. Health
7 November 2013

When blood vessels go wrong, why are we better at treating the heart than the head?

The strange discrepancies between how we treat strokes and heart attacks.

By Phil Whitaker

When I started practice in the early 1990s, medical attitudes to strokes and heart attacks couldn’t have contrasted more starkly.

Heart attacks were often dramatic and challenging; there were plenty of treatments to deploy, and much high-tech gadgetry to play with. Good outcomes were immensely satisfying, a confirmation that medicine made a difference. A stroke, on the other hand, felt like a depressing fait accompli. There was little to be done by way of treatment, survival was a matter of chance, and many patients were left with profound disabilities from which any recovery was painstaking and marginal.

The pathology underlying the two conditions is broadly similar. Every organ relies on uninterrupted perfusion of blood for its oxygen and nutrition. Clearly blood has to be liquid in order to circulate, yet it is also chock-full of tiny platelet cells, and a soluble chemical, fibrinogen, that will solidify into a clot at a moment’s notice. Blood vessels are lined with the biological equivalent of Teflon – the vascular endothelium – which ensures this clotting potential is held in check. Any breach in this endothelium activates the platelets, causing them to clump together in great numbers and to convert fibrinogen into its insoluble cousin, fibrin, which coagulates into a matted web.

This clotting cascade is vital in trauma, sealing damaged vessels and limiting blood loss; but when it is triggered in other circumstances, it can have catastrophic effects.

Cholesterol-rich plaques in arterial walls – the “furring up” of popular discourse – can swell and rupture the vascular endothelium. The ensuing clot may block the vessel entirely, causing death to the tissues downstream. If this occurs in a coronary artery, heart muscle dies – a myocardial infarction (MI), or heart attack. In the brain, the result is a stroke.

In the UK, deaths due to MI halved between 2002 and 2010. Some of this dramatic drop is because heart disease is becoming less common, thanks to the decline in smoking, and improvements in diet and exercise. The NHS has also become better at identifying and offering preventative medication to those at high risk. But around 50 per cent of the astounding increase in survival comes down to the transformation in treatment of those who have the misfortune to suffer a heart attack.

The management of MI has been revolutionised by techniques to unblock occluded coronary vessels, thereby salvaging as much of the blood-starved heart muscle as possible. The earliest attempts used “clot-buster” drugs known as thrombolytics, which cause the fibrin in the offending clot to dissolve. Thrombolytics still have an important place, but surgical approaches are ever more commonplace.

Angioplasty, where a wire is threaded up to the coronary vessels from an artery in the groin, has become the first-line emergency treatment for the most serious types of MI. A balloon at the end of the wire, or an implantable wire cage called a stent, can be deployed to reopen the blocked vessel.

Time is of the essence: the earlier that perfusion can be restored, the less heart muscle will die, and the better the outcome (in some cases, MI can actually be aborted). Ambulance services, and A&E and cardiology departments, have refined protocols for fast-tracking suspected MI sufferers, and “door-to-needle” or “door-to-balloon” times have been reduced substantially.

Stroke medicine has also undergone a revolution in recent years. Thanks to a sustained research effort led by the Stroke Association, much more is understood about maximising recovery following stroke, and most sufferers will now be treated in a dedicated stroke unit, which significantly improves outcomes.

The holy grail, though, would be comparable success in re-perfusing blood-starved tissue after stroke to what cardiologists are achieving in MI.

Stroke is different in a number of ways. Angioplasty is not useful in the majority due to the small size of the vessels within the brain. Thrombolysis should, in theory, be successful – but whereas re-perfusion can salvage heart muscle up to 12 hours after the onset of symptoms, brain tissue has a much narrower window of opportunity, probably around three to four hours.

And not all strokes are caused by clot. Around one in ten occur when a blood vessel ruptures and bleeds into the surrounding brain; you most certainly don’t want to give clot-busting drugs in those cases. They can be identified on a scan, but more challenging to predict are those patients suffering a clot-induced stroke who go on to bleed into the damaged neural tissue, something thrombolytics also make catastrophically worse.

The balance between benefit and harm is a fine one, and some experts have recently called for thrombolysis in stroke to be confined to clinical trials until the evidence to justify its use is clarified.

For now, at least, we continue to rescue the heart more successfully than the head.

Phil Whitaker is an award-winning novelist and a working doctor