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The Science behind Allergy

Rheumatic Patches

Dr David L. J. Freed, MB, MD, MIBiol
Allergy Information Sheet 10

"Lumbago", "muscular rheumatism", "fibrositis", "creaking gate", "not as young as I used to be". Ordinary folk seem to understand very well what these things mean but doctors have difficulty in finding any real pathology. We prescribe analgesics, rub-on counter-irritants and cheerful reassurance. Pharmacists do a roaring trade in over-the-counter remedies, and while all this is going on the nation suffers a huge weekly loss of its workforce because of low back pain The joints, by and large, are not affected. Arthritis can occur also in the same patient, but seems to be a later thing, supervening only after years or decades of pain, which originally seems to lie in the muscle bellies. Painful patches of soft tissue are common, affecting well over half of the "normal" population. They are frequently "inadvertently discovered by patients, their spouses, therapists, and non-medical practitioners" (1), but rarely by doctors, who have been taught to examine the bones and joints only. This is because the painful muscles show no pathology. Numerous histological studies have failed to discern any definite pathological changes in the muscles, so the whole disease is consigned to the netherworld of "symptoms without causes", somatization, hysteria, and other unprovable neopsychiatric ephemera.

The joints, by and large, are not affected. Arthritis can occur also in the same patient, but seems to be a later thing, supervening only after years or decades of pain, which originally seems to lie in the muscle bellies. Painful patches of soft tissue are common, affecting well over half of the "normal" population. They are frequently "inadvertently discovered by patients, their spouses, therapists, and non-medical practitioners" (1), but rarely by doctors, who have been taught to examine the bones and joints only. This is because the painful muscles show no pathology. Numerous histological studies have failed to discern any definite pathological changes in the muscles, so the whole disease is consigned to the netherworld of "symptoms without causes", somatization, hysteria, and other unprovable neopsychiatric ephemera.

More recently, in a welcome attempt at clearing away some of the confusion, the American College of Rheumatism has proposed to term fibromyalgia (2). This "diagnosis" is not actually a diagnosis but a descriptive label, meaning pain in the muscle fibres (the more traditional term "fibrositis" had finally to be abandoned as there simply is no inflammation to account for the pain). Fibromyalgia is now defined as a condition in which the patient experiences pain in all four quadrants of the body, where firm palpation in certain designated areas will elicit tenderness. These areas include the trapezii, the occiput, medial and lateral epicondyles, buttocks, and inner aspect of knees. The American College is earnestly seeking to prise control of fibromyalgia from the hands of the psychiatrists, and most psychiatrists would be happy to let them do so, but general physicians still find it hard to accept fibromyalgia as a "real disease" and treatment remains unsatisfactory (3). But there is real pathology to be seen. The trouble is, as so often, that until recently we were all looking in the wrong place.

The late Dr W.W. Fox, during his long clinical lifetime (over 60 years in medical practice), followed up rheumatic patients, with and without arthritis, for decades (4). He observed, in every case, the tender patches in soft tissues that we have been considering. Particularly interested in low back pain, he passed.long needles down through the skin in the lumbar area, down to the psoas, in several patients, seeking the area of maximum tenderness. The response was startling. The main pain was not in the muscles, not in the bones, not in the joints, not even in the bursae or ligaments. It was in the skin, and the loose connective tissue (superficial fascia) just under the skin.

It is astonishing that an organ as obvious and exposed as the skin seems somehow to escape notice most easily. This is probably because rheumatic patches are in the dermis. The dermis is a mesodermal organ while the epidermis is ectodermal. The epidermis has a very rich nerve supply and exquisitely accurate touch localisation, whereas the dermis, like other mesodermal structures, has neither. Sensations arising from the dermis are interpreted by the brain only as “deep to the surface”.

To the casual eye the affected area of skin looks normal. On closer examination there may be a patch of tiny "thread veins", expanded capillaries, to be seen. There may also be one or more "skin tags" - benign papillomata - whose histology is the same as the underlying rheumatic patch (see below) and which is surprisingly tender when you tweak it. When there is a rheumatic patch overlying the back of the neck at C7 level, there may be an exaggerated forward curvature of the neck (the so-called "dowager's hump"). A rheumatic patch in the scalp may cause the overlying tuft of hair to stand at a different angle from surrounding hairs. But most of the time rheumatic patches are invisible; the abnormality can be felt by the educated fingers of the enquiring examiner, but not seen. Occasionally the patient knows exactly where the rheumatic patch is, and can place his finger on the spot, but this is rare. For most of the time he is unaware of its existence, and is astonished when your pinching fingers make him yelp.

Look for rheumatic patches in all patients with pain, irrespective of whether the pain is perceived to be in the joints, the muscles, the head or face. The classic place is the skin overlying the trapezii, the ledge of flesh that extends sideways and downwards from the base of the skull to the shoulders. Pick up a shallow skinfold and roll it gently between your thumb and fingers. Compare the sensation with other areas, or (better) with the skins of gymnasts or runners, who are rarely affected. With luck you will find at least some rheumatic patches on your own body, and can compare the sensation in different areas with the painfulness or otherwise of the pinch. It is important to pinch up a skinfold as shallow as possible, and squeeze it sideways, parallel with the skin surface. Then try pressing directly downwards. The sideways pinch is far more tender than the downwards press, proving that it is the skin that contains the problem patch, not the underlying muscle.

Clinical Manifestations

Most forms of arthritis, especially osteo and rheumatoid, will be found to be associated with rheumatic patches. Treating these alleviates the pain to some extent, even when arthritis is quite advanced, and Fox believed that prolonged rheumatic-patch treatment can even halt or reverse the arthritis (4).

Migraine and tension headache will show rheumatic patches in the scalp and face. Patients (and doctors) often ascribe these headaches to "stress". Nonsense. Everyone has stress in his life; I have stress, you have stress. But not everyone gets headaches from it. There has to be another factor involved, as well as stress. There is. It is called the rheumatic patch, and that in turn is caused by dietary and other environmental factors (see below).

Many patients with vertigo and tinnitus have rheumatic patches in the scalp behind and above the ears.

Acute stabbing pains in the head and face, which we tend to ascribe to "neuralgia" (whatever that means) are caused by rheumatic patches (with the possible exception of true trigeminal neuralgia, which I have little experience of). You may not be able to demonstrate them by squeezing, since the skin and scalp in those areas are too tightly tethered to pinch up, but you will know when you insert your needle (see below), and the patient will know, straight away, when your injection abolishes his pains.

Acute wry neck - sudden pain in the trapezius area brought on by some trivial movement of the shoulders, and thought to be due to a "trapped nerve" ("axonotmesis") - is always in fact associated with an exquisitely tender patch of skin in the painful area. The patient will be astonished when your pinching fingers locate the patch; he is more inclined to believe that the muscle has been torn. It is immensely rewarding when a quick (though horribly painful) injection into the skin of the neck abolishes the "trapped nerve" within minutes. Why the rheumatic patch in that spot should have flared up instantaneously following a trivial movement I am not sure; I suppose that being abnormally stiff, the patch must have sustained a tear there. Alternatively, in view of the abnormal electrical characteristics of these patches, perhaps there has been some acute electrical discharge. Sudden pains of this kind are also common in the lower back. The patient can pinpoint the movement that caused it and is certain that a disc has slipped or a muscle is torn, but he is usually wrong. Prolapsed discs do occur, but much more rarely than you think.

The "sacroiliac strain" so beloved of sports physiotherapists and those who advise women before and after childbirth is actually due to rheumatic patches in the lumbosacral area.

The various occupational conditions falling within the category of "repetitive strain injury" will be found to have rheumatic patches close to or overlying the painful area. A musician, for example, will get pain in the wrist which will disappear when you treat the rheumatic patch in the volar forearm. In these cases the patient will often pinpoint the area accurately, but will be astonished to find that a treatment affecting the skin alone will alleviate pain that he had thought came from deeper inside. Repetitive strain is a normal feature of life. Only people with abnormally stiff skins and connective tissues suffer pain from it. The same is true of the neck/back pain that may follow sleeping in an awkward position; had there been healthy skin, there would have been no pain. Migrating geese get a fair bit of "repetitive strain", but they rarely seem to drop out of the sky from pain in the wishbone.

You may be surprised how many cases of "prolapsed disc" and sciatica show rheumatic patches, and how many respond to skin treatment. Never make a firm diagnosis of slipped disc without a myelogram or CT scan - half of the patients with typical symptoms have pretty normal discs, but abnormal skins, and these are the ones who are so easy and gratifying to treat.

"Whiplash injury", if it lasts more than two weeks, and especially if the history indicates that the pain began some hours after the accident, is caused by rheumatic patches in the painful area. Pre-existing mild rheumatic patches that were causing no trouble are often aggravated by relatively minor trauma, such as a fall or banging the head; the pain seems out of all proportion to the injury and often begins only a few hours afterwards. Wait for a few weeks, to see if the pain will go by itself, then treat any remaining painful patches as explained below.

Muscle fasciculation, cramps, and neuralgias may also be caused by rheumatic patches, due to the abnormal electrical properties of these areas of skin (see below), though my experience is limited in these conditions and I am not yet sure. It seems likely to me that Ekbom's syndrome (fidgety legs) will be found to be mediated by the abnormal electrical properties of the superficial fascia of the calves; rapid shaking of the limbs serving to normalise the charge.

Rheumatic patches do not always cause pain. They may be completely asymptomatic, or only slightly tender. Probably most people have some mild patches, but they are not severe enough to cause trouble. Alternatively, the main symptom may not be pain exactly, but itch, tingling, stinging or hyper/paraesthesia. "Carpal tunnel sundrome" is not due to the possession of a carpal tunnel (all of us have those), but to the oedema that sometimes collects in or distal to a rheumatic patch.

Look for rheumatic patches wherever there is musculoskeletal pain, whether or not there is also a conventional explanation for it. Worthwhile palliation can almost always be achieved, in all of the examples listed here, by injection therapy (see below). You will be surprised how much general glumness, moodiness and depression you can alleviate at the same time.

Biophysics and Biochemistry

All organs of the body, from epidermis in, are covered by and penetrated by connective tissue. All of the body cells, except for those of the blood and lymph, are surrounded by and to some extent supported and immobilized by connective tissue. The dermis itself is a somewhat condensed connective tissue, merging imperceptibly into the loose connective tissue that lies immediately beneath it (the superficial fascia). The connective tissue forms a complete organ on its own; every part of it is in direct continuous communication with every other part. It is also piezoelectric - when deformed, an electric charge is set up (5). That, presumably, is why when you squeeze a rheumatic patch in the skin of the shoulder, the patient sometimes complains that the pain radiates down to his fingers - or why squeezing the forearm skin may cause him to experience pain in the groin! Because of the abnormal bioelectricity of rheumatic patches, I find it easy to believe that a nerve traversing such a patch of tissue might be inappropriately stimulated, causing either neuralgia or muscle cramp/fasciculation, depending on whether the nerve is sensory or motor.

The physical property of connective tissue is to be sticky, semi-fluid and semi-solid, and flexible. It must be firm enough to hold the organs in place, but fluid enouqh to allow appropriate movement. Connective tissues range in consistency from the hard and inflexible (cartilage, tendon) through to the very soft and wobbly (mammary stroma), but all connective tissue matrix is made up of two basic components with interspersed cells: (1) a carbohydrate-rich gel; (2) criss-cross "ropes" of collagen and elastin. The only basic difference between hard and soft connective tissues is the relative proportions of these two basic components (5).

Connective tissue is therefore an example of what structural engineers call a "composite material". Another example, apparently totally different but actually rather similar, is reinforced concrete, in which the concrete is given extra strength and some flexibility by steel bars embedded in it. The steel bars must be adherent to the surrounding concrete. If rust penetrates, separating the bars from the concrete, the structure loses its strength and the bridge collapses. The greater the adherence between the bars and the concrete, (or between adjacent bars) the less flexible and more stiff the material becomes. These remarks apply to connective tissues and skin just as they do to concrete.

All composite materials share certain physical properties. One of these is the distribution of stresses.

A structure made from a material is held in shape by forces which either push or pull bits together or push or pull them apart. A familiar example will be a tent. The forces on the tent pole are (a) the weight of the canvas trying to push it into the ground, (b) the resistence of the ground pushing up against this, and (c) the sideways pull of the canvas and guy-ropes. Hopefully, all of these forces will balance each other so that the tent stays up. If we now examine the materials more closely we will see that these forces are not evenly distributed. The tension on the canvas, for example, is most concentrated around the attachment of the guy-ropes (the manufacturer will often reinforce these areas to allow for that). Lines of equal force are termed stress trajectories.

It is a property of all composite materials that the stresses concentrate in the stiffest areas. These are the areas that will fail if we keep on increasing the load on the material, even, paradoxically, if they are stronger than the surrounding material, because they take a disproportionate share of that load.

When we stand erect we pull our shoulders and head backwards to counteract gravity which is always tending to pull us forwards (the centre of gravity of the head and thorax normally lie in front of the mid-line). The lumbar spine is pulled into its proper curve (lordosis) by the muscles between sacrum and thorax, and the neck is pulled into its correct backward curve by the muscles between shoulders and occiput (principally the trapezii and sternomastoids). Normally the entire weight of head and thorax are supported by these muscles and the associated tendons. The skin and subcutaneous connective tissues, which in health have plenty of flexibility, take little or none of this load. But when the skin and superficial fascia become stiffer, the stress trajectories start to concentrate in these stiff areas, which not being designed to take such a load, hurt. Pain in the back, shoulders and neck that is not explained, or insufficiently explained, by pathology of the spine and spinal joints, is usually due to rheumatic patches. These affect all areas of the body but do not usually hurt except in these dorsal areas, because those areas are where the stress trajectories are most concentrated. It is certainly possible to get rheumatic-patch pain ventrally, but much less common.

When the stiffness of a rheumatic patch is abolished by effective treatment (see below), the stress trajectories instantaneously become redistributed to other stiffened areas, which then start to hurt instead. Overall treatment is aimed at gradually softening all rheumatic patches, following the migration of the maximal pain.

Histologically, rheumatic patches show an appearance somewhat reminiscent of scleroderma, in that the markings of collagen bundles become fainter, the distribution of collagen bundles becomes more haphazard, hair follicles and sweat glands are diminished, and there is some infiltration by lymphocytes (6). There is often oedema in the affected area, which resolves very rapidly on treatment (see below).

Why then do skin and connective tissues become affected in this way? Various hypotheses have been advanced (6). To my mind any useful hypothesis must take account of the dietary connection. Fibromyalgia (rheumatic patches) is a common feature of Chronic Fatigue Syndrome ("myalgic encephalomyelitis" or "ME") and is responsible for the "myalgic" (= muscle pain) part of that life-ruining condition. It responds to diet and desensitization along with the other symptoms.

Of the various rheumatogenic foods, wheat and other grains top the list. Avoidance of these is frequently the only dietary maneouvre required, especially in early cases. Wheat and other grains contain lectins (7) having an affinity for the monosaccharide N-acetyl-glucosamine(GNAc).

Connective-tissue and skin proteoglycans have considerable quantities of this sugar and bind wheat lectin strongly (8). Wheat lectin is highly resistant to cooking and digestion and survives passage through the gut (9). My hypothesis proposes that ingested wheat lectin (and other dietary lectins) enter the bloodstream from the intestine and bind to the connective tissues, making them abnormally stiff. The biophysical consequences of that abnormal stiffness have been explained above.

While the lectin hypothesis is unproven for the time being, some remarkable and unexpected support for a role for wheat lectin in rheumatoid disease has come from studies on the biochemistry of antibodies. Antibodies of the IgG class have carbohydrate side-chains which normally terminate in galactose. The IgG molecules in rheumatoid disease is defective; instead of terminating in galactose they terminate with N-acetyl-glucosamine - the very sugar for which wheat lectin is specific.

Of four biopsies of rheumatic-patch skin submitted to an independent pathologist in 1987, two had been taken from patients of mine who had been on wheat-free diets, and were improving, but still had some pain. The pathologist commented that these two biopsies were different from the others, being more circumscribed and less extensive than the other two.

It may also be noted that a common trigger for a relapse of rheumatism and arthritis is an attack of flu. Fox, in originally noting this association, speculated that the flu virus must invade the skin and connective tissues directly. Virological investigation of rheumatic patches has however been negative so far. It occurs to me, in support of my lectin hypothesis, that influenza viruses possess a surface enzyme, the neuraminidase, which clips the terminal neuraminic acid (synonym: sialic acid) from the glycoprotein coating of cells, making them more susceptible to binding by lectins. According to this hypothesis, therefore, influenza viraemia need not affect the connective tissue directly; all it needs to do is make the tissues more sensitive to any dietary lectins that happen to be there at the same time. This makes the ancient naturopathic practice of "starving a fever" suddenly a lot more sensible.


As mentioned above, wheat avoidance may be enough to alleviate the pains in early cases. In longer-standing cases a full stone-age diet will gradually achieve the same result, although it may take many months and be preceded by an aggravation of pain. This seems to occur together with the diuresis that frequently occurs in the early stages of the diet, presumably because the connective tissues are no longer distended by excessive water.

As a short-term first-aid measure, intradermal injections of a suitable chelating agent are very rapidly effective. This is because chelating agents uncouple the chemical links between collagen molecules and the carbohydrate matrix (10). This has the effect of softening the whole tissue, just as in the case of the rusty reinforced concrete noted above.

A suitable chelating agent for clinical use is 0.5% sodium salicylate in physiological saline. The injections are painful, so it is merciful to add some lignocaine to a final concentration of about 0.2%. Trisodium EDTA, in the form of Limclair injections at 1%, is more effective but also more painful, and gives rise to worse bruises. Sodium salicylate injection, strangely, is classified as an unlicensed medicine in the UK and the doctor must use the exemption scheme (inquire of the Medicines Control Agency).

One advantage of using salicylate is that at 0.5% it only hurts when your needle is in a rheumatic patch; normal skin does not hurt and this guides the operator. Another guide is the sensation of resistance that you get when sliding the needle into the skin; normal skin does not resist the needle tip, but when the needle is in a rheumatic patch you get a sensation of resistence both when advancing and when retracting the needle. It feels rather like drawing a bow across a violin string. An injection of 2-3 ml intradermally will treat an area of around 2 cm diameter, and the symptomatic improvement is usually felt within a few minutes. Some patients do not feel better immediately; they may need to go home and sleep first. It is always worth asking the patient if he feels better immediately following the injections, but be prepared for the odd one who does not feel better till next week. Use as many objective measures as possible - how far can he slide his fingertips down his straight legs, how strong is his grip etc - as patients' perceptions are subjective and they may be surprised how much more movement they have immediately after the injection.

Beware of the phenomenon of mobile stress trajectories mentioned above; as you treat one area the pain will almost immediately move to another area, and the patient may be conscious only of that and not of any improvement. Nevertheless, you may reasonably expect at least some degree of improvement every time you inject rheumatic patches.

After injecting scalp rheumatic patches for headaches, do not be surprised if the patient experiences one last awful headache a couple of days later. It will often be the last headache he gets.

Unless you have the patient on a suitable diet at the same time, the improvement will be transient, although it may last for months. In active cases the improvement will only last minutes, making the injection treatment worthless for practical purposes.

There is no doubt in my mind that psychological factors are also highly significant in amplifying the pain of rheumatic patches, and these can be strong enough to transform a pain that would hardly have been noticed into crippling fibromyalgia. But without rheumatic patches there to start with, there would be nothing to amplify – like turning up your radio to maximum volume when there is no signal coming in from the transmitter.


1) Cailliet R (1983): Foreword, in Travell JG and Simons DG (eds): Myofascial Pain and Dysfunction; the Trigger Point Manual, Williams and Wilkins, Baltimore, p xi.
2) Wolfe F, and the Multicenter Criteria Committee (1990) The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Arthritis and Rheumatism, 33: 160-172.
3) Ahles TA, Yunus MB, Masi A (1987): Is chronic pain a variant of depressive disease? The case of primary fibromyalgia syndrome. Pain, 29: 105-111.
4) Fox WW (1981) Arthritis: Is Your Suffering Really Necessary? Robert Hale, London.
5) Hukins DWL, Aspden RM (1985) Composition and properties of connective tissues. Trends in Biochemical Science, 10: 260-264.
6) Fox WW, Freed DLJ (1990): Understanding Arthritis: The Clinical Way Forward. Macmillan, Basingstoke, pp 29-32.
7) Freed, DLJ (1985) Lectins (signed leading article), British Medical Journal, 290: 584-6.
8) Freed DLJ (1991) Lectins in food: their importance in health and disease. Journal of Nutritional Medicine, 2, 45-64.
9) Brady PG, Vannier AM, Banwell JG (1978): Identification of the dietary lectin, wheatgerm agglutinin, in human intestinal contents. Gastroenterology, 75: 236-9.
10) Steven FS (1967): The effect of chelating agents on collagen interfibrillar matrix interactions in connective tissue. Biochimia et Biophysica Acta, 140: 522-528.

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