By Dr. Charles Shepherd
In view of all the recent discussion about areas of overlap between ME (Ramsay described), CFS (Fukada et al research criteria) and FMS/fibromyalgia syndrome (American College of Rheumatology criteria) here are what I believe are some of the key areas of similarity and difference:
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All three conditions have clinical features in common. These include post-exertional fatigue/malaise, cognitive dysfunction, paraesthesiae or hypoaesthesiae/numbness, headaches, sensitivity to noise and bright lights, alcohol and medication intolerance, non-refreshing sleep, problems with temperature control, irritable bowel and bladder symptoms. And this is why someone with this sort of symptomatology might then be labeled as having ME (by a doctor who accepts there is a clinical difference between ME and CFS), CFS (by most specialists who regard ME and CFS as exactly the same) or FMS (mainly by rheumatologists). My personal preference is to use whichever term seems most appropriate from the point of view of the clinical symptoms and then say ME or CFS plus a fibromyalgic component if a patient with ME or CFS has musculoskeletal pain (rather than nerve pain) and some of the characteristic tender spots on examination which are so typical of FMS.
But there are important differences between the three conditions. For example, you must have musculoskeletal pain and at least 11 out of 18 specific bilateral tender spots (to assess this the doctor should use his thumb to press into the skin) if you are going to meet with the strict diagnostic criteria for FMS (there’s an illustration of where these tender points are on p107 of ‘Living with ME’). A significant minority of people with ME and CFS don’t experience pain (muscular, joint, or nerve) at all whereas others have pain which varies from mild to severe and persistent to intermittent. FMS also tends to come on gradually rather than follow an acute infective episode (although it can be precipitated by acute trauma such as an RTA). And unlike ME or CFS, there is an association between FMS and other rheumatic conditions such as lupus or rheumatoid arthritis, as well as inflammatory bowel disease.
As far as possible pathology is concerned, the latest thinking on FMS is that besides sleep disturbance being an important factor, the underlying cause may be an abnormality in the central nervous system related to pain processing as increased levels of a substance called P3 have been found in the cerebrospinal fluid of FMS patients. As with ME and CFS, areas of cerebral hypoperfusion can be shown using neuroimaging (i.e., SPECT scans).
For some people with FMS a rather more active approach to activity management seems to be helpful – but it doesn’t work for everyone. As with ME and CFS, a low dose of a sedating tricyclic drug (e.g., amitriptyline) is often prescribed for pain and sleep disturbance. In FMS there’s also some evidence to show that a flexible regime which combines amitriptyline and fluoxetine (both started separately at the lowest possible dose) can be beneficial.