Sir William Richard Gowers (1845-1915) was a British neurologist. In 1904 he published in The British Medical Journal and article titled LUMBAGO : its Lessons and Analogues. In that article, he suggested a general term, “FIBROSITIS”, to designate this type of non-articular rheumatism. From then the term “fibrositis” was used by many physicians and has led to many controversies, discussions and misunderstandings. Personal note: despite GOWERS explains clearly that he related the symptoms of lumbago (especially the impossibility to move) with the affection of the FIBROUS TISSUE that surrounded the muscle spindles, that fact was OMITTED and was just related to fibrous tissue in general.

Gowers’ first intention was to recall attention that may be the primary lesions in the “muscular rheumatism” called lumbago were not in the MUSCULAR tissue itself, but in the FIBROUS TISSUE that surrounded the MUSCLE SPINDLES and that of the tendons and aponeurosis. He explained the knowledge that they had of these sensory organs of the muscles (muscle spindles) and the tendons by then and correlated the dysfunction with the symptoms.

Personal notes: It seems to me that Gowers’ term “fibrositis” was just a proposal with the intention to recall attention to the fibrous tissue as the origin of pain, but it seems that he was such a recognized neurologist that his suggestion was taken immediately by the medical community, especially in England. Personally I think it was a wrong name. In medicine –itis designates and implies INFLAMMATION (inflammation with its clinical cardinal signs with heat, redness, swelling, pain, and loss of function, and “inflammatory products” or histological findings). Later, the histological findings did not correlate that. After a period of “fibrositis fever” and many discussions (The Harveian Society of London Lecture in 1913 and Swansea Congress in 1965) from the middle 20th century, the term was abandoned gradually by the community. In this article he made an effort to clarify that this “rheumatic inflammation” would not present as the “typical inflammation”, but more like a VASCULAR DISTURBANCE. But it seems that all these explanations were no further read.

It is noticeable to realize that Gowers introduces his lecture by wondering –more than 100 years ago– what was really the cause of lumbago or stiff neck. Surprisingly, for the majority of us physicians, it’s still unknown.

Gowers’ article is written in an exquisite English language manner.

Personal notes about the article:

A Lecture on Lumbago: Its Lessons and Analogues.

Delivered at the National Hospital for the Paralyzed and Epileptic.

Br Med J. 1904 Jan 16; 1(2246): 117-21.

PubMed PMID: 20761312; PubMed Central PMCID: PMC2352601.

ARTICLE FREE ON LINE

//www.ncbi.nlm.nih.gov/pmc/articles/PMC2352601/pdf/brmedj08152-0001.pdf

Gowers himself admits to have suffered lumbago

Gowers delivered this lecture at the National Hospital for the Paralyzed and Epileptic. He started his lecture about lumbago saying:

“Gentlemen, there are many ways of acquiring knowledge of disease. Perhaps the most effective -although certainly the least agreeable- is PERSONAL EXPERIENCE”.

He also warns the audience that lumbago is so common that they would be exceptionally fortunate if they escaped to suffer it once in life.

Gowers wonders: WHAT IS LUMBAGO?

He admits that all the physicians have a clear view about the symptoms. BUT HE ADMITS THAT THE ETIOLOGIC NATURE IS NOT CLEAR.

By then they considered lumbago to be a type of MUSCULAR RHEUMATISM. Also another old term was “myalgia” (not in use anymore).

Gowers started analyizing “the symptoms of lumbago”:

The main symptom is PAIN in the lumbar muscles.
PAIN is felt only when the muscles contract or extend.
In health we are conscious of no sensation in the muscles (despite there may be certain afferent unconscious impulses).

Gowers stated that in certain occasions we must all have been made aware of such afferent impulses when they are rendered intense by the excessive contraction, called “cramp”. Therefore, the intense stimulation causes severe pain. It also renders the muscles afterwards over-sensitive, and further tension may cause pain.

The afferent nerves that can lead to pain in the “muscle spindles”

These nerves do not end in the “normal” muscular fibers, they end in the INTERSTISIAL TISSUE, where there is FIBROUS tissue between the fibers, in the “muscle spindles”. And from there there must be constant unperceived afferent impulses in health conditions from these afferent nerves.

Gowers’ notes about the knowledge of the muscular spindles and its relation to lumbago spindles

-“Muscle spindles” could explain the acute pain – while acute maintained contraction-by afferent nerves:

-“The muscles spindles” are long bodies lying between muscular fibers.

-The “muscle spindle” has a fibrous capsule.

-The “muscle spindle” would act as a “muscle-meter” structure.

-Maybe in acute compression they could give rise to acute pain.

-Strong stimulation of any afferent nerves could cause pain.

Gowers hypothesized about the muscle spindles giving rise to pain in lumbago

Gowers hypothesized that a state of extreme sensitiveness of the “muscle spindles” could explain the lumbago. He then emphasizes that the “muscle spindles” apparently belong to the FIBROUS TISSUE since a fibrous capsule surrounds them.

Gowers’ notes about fibrous tissue

Fibrous or connective tissue is an element common to all structures and organs.

It seems to be related to certain morbid states, especially it seems to be susceptible of what they called “rheumatism”.

So Gowers insists that the lumbago, as part of a rheumatic malady, has its nature in the fibrous tissue (where the “muscle spindles” lie), rather than in the muscular tissue itself.

Another proof that lumbago is related to the fibrous tissue is that pain spreadsto the tendinous attachments of the muscles to the iliac crest bone and the back of the sacrum. Contraction of the muscles causes tension in these tendinous structures, which also have nerve endings that resemble muscle spindles in peculiar bodies enclosed in capsules that react to the increasing of tension of the tendinous structures.

Gowers uses the concept of “tendinous lumbago” and “sacral lumbago” to explain this fibrous tissue involvement in the lumbago pain. He even said that through the fascia it spreads and can reach the fibrous sheath of the sciatic nerve causing sciatic neuritis, at the end the inflammation reaches the nerve and can cause muscular wasting and diminution of sensibility.

Gowers defines the muscular rheumatism as an inflammation process of the FIBROUS TISSUE of the muscles, tendons and aponeurosis by spreading.

GOWERS THEN “invents” the term FIBROSITIS as analogy to “cellulitis”

He correlates that the inflammation of the “looser cellular tissue” by septic influences was called “cellulites”, and then there is inflammation, induration, and suppuration.

Then he proposes that there could be a term that designates an inflammatory process but without suppuration. For analogy to “cellulitis”, he invents “fibrositis”.

Nevertheless, he insists that fibrositis differs from ordinary inflammation, since there are NOT “inflammatory products” as suppuration or “hyperplastic process”, BUT HE COMMENTS that the vascularity is CONSPICUOUS. So he suspects that the vessels of the fibrous tissue and the muscles probably share an acute disturbance. What he named “rheumatic inflammation”.

Gowers also recalls another particularity of lumbago, which is the EXTREME SUDDENNESS with which symptoms seem to come on

The patient usually experiences the transfix pain which makes the movement impossible:

ON THE FIRST MOVEMENT AFTER A PERIOD OF REST
FIRST MOTION IN THE MORNING
WITH A PREVIOUS GRADUAL DISCOMFORT AND THEN WITH A PARTICULAR ACTION CAUSES AN EXTREME DISCOMFORT.

Gowers hypothesizes that the pain may come suddenly, but the underlying condition may have developed gradually.

Neuralgia was used to designate SPONTANEOUS PAIN (not related to movements), that’s why GOWERS does not like the term “myalgia” for the muscular rheumatism since it would give this sense of spontaneity.

Gowers also recalls attention on another entity, he called it “MUSCULAR FIBROSITIS OF THE ARM” or brachial fibrositis

Maybe it had other names, such as brachial myalgia. It presents as severe pain at any movement of the arm, the joints of the shoulder, the elbow, and even the wrist, which seem to be affixed. Every attempt to move is prevented by a secondary contraction in the muscles so painful that can make “a strong man cry out”.

BUT YET IF THE patient does NOT know what you are doing, and one proceeds with such gentleness that the movement is really imperceptible, one can be surprised how much PASSIVE movement is possible.

Gowers explains an example of a patient whose doctor thought that he had a FIXED SHOULDER, by moving slowly the arm he could move step by step up to a considerable degree. Similar experience with the wrist (the muscles present a contraction that can be won by slow manipulation).

He warns that maybe sometimes the pain seems to be spontaneous because in every position there is always a degree of contraction or tension, sitting or laying, but the pain is really caused by the movements.

Gowers states that in cases of “severe brachial fibrositis” there may be a secondary brachial neuritis with clear consequences: tenderness of the nerves along their course and their distribution, hand edema, muscular wasting, or impaired sensation (RARE IN SECONDARY NEURITIS).

OTHER considerations

Other examples of fibrositis:

Stiff-neck
Pleurodynia (intercostal fibrositis)

He also noticed that fibrositis of the back tends to be bilateral but affecting one side more than the other, and it spreads to the sciatic nerve on the side that is more severe.

He also remembers that the “muscular rheumatism” is more often in the second half of life, in contrast to “acute articular form”, which is more common in early ages.

He also comments on the relation to these entities with the finding of gout, despite he insists that it “would be gout with a difference”.

FIBROSITIS related to PAST TRAUMA, pain after a STRAIN

That would be another form of fibrositis induced by a SUDDEN VIOLENT tension on the tendinous and ligamentous structures.

He remembered a woman that had an accident and strained her back severely during an overturning of a tramcar 3 months before. Since then, she had extreme sensitiveness of the tendinous attachments of the dorsal muscles to the iliac bone. Pain limited her movements a lot. It seemed to Gowers that the muscles of the lower back and sacrum were especially prone to such traumatic derangement. Some sensitiveness to pressure also coexists, but pain is much worse with tension movements.

Gowers hypothesizes that maybe in the early stages after the trauma there was a more “normal inflammatory process”, but later it may be more a residual effect.

He differs that slighter forms of “muscular fibrositis” such as “lumbago or stiff neck” from the “tendinous forms” may last much longer. Gowers states: “Somehow, it seemed that the duration of the muscular fibrositis is proportioned to the slowness of its onset”. Stiff neck can have an acute onset, and it seems it doesn’t last so long.

Treatment of the “rheumatic fibrositis” according to Gowers:

–DIAPHORESIS: the free perspiration has some popular recognition, it seems that muscular rheumatism may be cut short at its onset by active exercise. Exercise that does not involve the affected muscles and it causes COPIOUS PERSPIRATION. It seems to relieve the condition of the blood, and maybe enables the morbid state to quickly pass away.

For example, if standing or walking does not affect the lumbago pain, the patient takes a long walk with a thick overcoat avoiding any chill, and the lumbago can be gone the next day.

A Turkish bath is equally beneficial and safer. But it is only at the onset that the relief is effective.

After 2-3 days, the muscular fibrositis seems to become so established that it cannot be speedily influenced by diaphoresis.

–REST: in the case of brachial fibrositis it should be with the use of a sling. NO PAINFUL movements should be done.

Other treatments:

Electricity and liniments (belladonna and chloroform) can also be used in later stages.
He also mentions the benefits of “saline” in an empty stomach to “flush out” the pseudo-gouty cases.
Salicylates seem not to be so good as in articular rheumatism.
He also mentions the combination of salicylate of potash or lithia or of soda. Colchicum or perchloride of mercury in intense cases.
Brachial form can be extremely obstinate; he comments the use of superheated air as treatment with its limitations.
The traumatic form of the tendinous fibrositis when it settles to a stationary condition can be resistant to almost all treatments.
A local measure that often does good is the DEEP HYPODERMIC INJECTION OF COCAINE, repeated daily for two or three weeks, probably eucaine would be equally effective by subsidence of the sensitiveness (Personal note: cocaine was used as a local anesthetic in the early years, prior to the development of other less toxic anesthetics).

Gowers’ final conclusions

Gowers admits that new studies with the use of microscope and modern techniques need to be done to get more evidence of the real nature of fibrositis.

He remembers that the “muscle spindles” and the tendon sensory elements have been recently studied and there are still other unknown structures. And he insists that the department of pathology should study this entity after discerning the “normal structure”.

Gowers is also aware that other life threatening maladies have received much attention.

Finally, he makes some sentences about the fact that the muscular fibers of the “muscle spindles” possess some independent vitality. Different from the rest of the muscle fibers that in case that the nerve is damaged, the normal muscular fibers and the muscle itself get atrophic, BUT not the muscle fibers of the “muscle spindle”, they seem to be independent.

Published in September 2018 By Marta Cañis Parera

REFERENCES

Gowers W. R. A Lecture on Lumbago: Its Lessons and Analogues: Delivered at theNational Hospital for the Paralysed and Epileptic. Br Med J. 1904 Jan16; 1(2246): 117-21. PubMed PMID: 20761312; PubMed Central PMCID: PMC2352601.