About Fibromyalgia

FIBROMYALGIA – THE BIOLOGY  PERSPECTIVE

Written by Romayne Wright BSc (Hons), DipNatSci (Open), Founder/Webmaster FMSNI

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If you’ve ever wanted to understand FM in the most basic of ways read on.  However, please note that this is only written based on being a sufferer and talking to many others over the years – talk to your doctor if you want expert knowledge/advice.  This article is a layman's perspective of Fibromyalgia. 

When you were told you had this weird strange named condition, you no doubt remember well, regardless of how long ago it was, how you felt.   You were probably confused as to what the diagnosis meant in reality – the consultant or doctor perhaps only telling you “it’s a muscle condition” or it’s “another name for fibrositis” or a type of “muscular rheumatism”.   Perhaps, horror of horrors your GP or Consultant suggested you start taking antidepressants - does he really think you're just depressed and it's all in your head still?   To try and take this down to a point where it’s easier to understand these issues require some very basic biology and I’ll start with the pain issue first.

You obviously are aware you have nerves all over your body and maybe you feel your entire quota are in your muscle tissue since that’s where most of your pain is arising from.  Well, pain is primarily a neurological (nerve to brain) response to stimuli e.g. trauma/heat/pressure etc coming from various sources within the body. In order to feel pain not only do these nerves require stimulation but they also utilise (neuro)chemicals to transmit the message to the brain through the nerves.   Nerves are like complex road systems – there are small fine ones and larger diameter nerves and they all end up in the spinal cord which is somewhat similar to a motorway in it’s ability to funnel all the nerves together into one place where the messages can then be transmitted rapidly to the brain. 

All you really need to be aware of is the obvious fact – when you stimulate a nerve ending you have a response – either cold, heat, pressure or pain depending on the nerve type and where it’s situated. Now when you touch your skin, you are aware of that sensation – how? 

The nerve endings in your skin (overlying muscles) are very sensitive to touch and pressure – when stimulated the tissues release chemicals that stimulate the nerves to transmit details of how much pressure has been applied or whether actual injury has occurred. See Figure 1 left (click on image for larger graphic).  The details transmitted by the nerves to the brain are then analysed and the brain determines your level of response, which would under normal conditions be the appropriate one e.g. if you only lightly touched yourself you’d ignore it or if you put your hand on a hot iron you'd rapidly remove it.  However, the case in Fibromyalgia is anything but  normal.    In our case, stimulation of our nerves results in a vast overreaction and hypersensitivity response whereby much more of the chemicals are released and sent to our brain, which can  do nothing other than tell us we’re in agony.  As far as it’s concerned light touch is heavy pressure, because that’s the message it’s getting via the (wrong) quantity of chemical being transmitted.  Now there isn’t just one chemical involved in this pain pathway – if there was, things would perhaps be much more simple.   You’ve most likely heard of serotonin, it’s one of the major chemicals now known to be involved in depression – well, it also happens to be very involved not only in the pain response  in conjunction with another important chemical (Substance P), but also in the correct functioning of many of our other major organs too as well as in promoting proper sleep – perhaps now you’re beginning to understand why it is that SO many   symptoms can be attached to this condition.  And also why depression can play a major role for many people.  We tend to be characteristically lacking in adequate levels of serotonin.  This is one of the main reasons why you will quite likely be offered certain antidepressants as a first line treatment for your condition. Most of the antidepressant drugs provided for FM starter treatments are called in the profession SSRIs – Selective Serotonin Re-uptake Inhibitors – all that basically means is that they enable the brain to maintain slightly higher levels of serotonin than it can otherwise manage on its own.   The important aspect of this is that your doctor won’t have prescribed (for most of you anyhow) antidepressants because he believes you to be depressed – rather he’s aiming to try and alleviate the sleep issue in an attempt to block the vicious cycle it perpetuates.   The dosage will be scaled appropriately – if you do state, however, that you are indeed feeling depressed, then obviously you need fuller treatment and thus your dosage of any antidepressant given may be higher than otherwise would be the case.   Another important thing to note on that score is that there is a wide range of these SSRI drugs – if you try the first one your GP provides for you for the requisite period (usually 6 weeks) and find it not making any dent in your symptoms, let your doctor know and they should be willing to try you on one of the others.

 

What I have said already is also part of the reason why the US researchers in particular have previously stated that they don’t foresee themselves coming up with an overall cure as such – the condition is too complex for them to formulate one pill to suit everyone.   Their philosophy is instead to target the overriding problem we all suffer from – pain.   One way of doing this is to try to prevent the pain message from reaching the brain.  Now this has to be carefully considered – a life without any pain whatsoever may sound great, but you have to remember it’s there for a purpose – to warn you of trouble and problems.   So, they can’t perhaps do what they’d really like to do to a great extent.   However, what they’ve talked about frequently is what’s termed an NMDA receptor blocker – yet another of the neurochemicals involved in the pain response pathway, and more importantly in the aspect of chronic pain.  Activation of NMDA receptors (these are just 'locks' that the NMDA 'key' fits into) has a number of important consequences. Because activation causes nerves carrying pain to be stimulated with less peripheral (e.g. from the skin) input, less glutamate (another important stimulus chemical) is required to transmit the pain signal, and more antinociceptive (blocking) input is required to stop it. Researchers feel that if you could block the different pain chemicals from activating these receptors then the message wouldn’t reach the brain.  Nice in theory – difficult in practice for a whole host of reasons. Although the research is ongoing in this area it may take some time yet to get it to a point where we can actually avail of it safely.