JMS Pearce
Hull, England

The accurate depiction of polymyalgia rheumatica (PMR) in the 1940s is relatively recent. By contrast, its close relative giant cell arteritis (GCA) was clearly described in 1890. Their early descriptions were separate and the recognition of their overlap did not appear until the 1960s.^1,2

The uncertain nature of the condition is shown by the varied names for PMR previously used: senile rheumatic gout, secondary fibrositis, periarthrosis humeroscapularis, peri-extra-articular rheumatism, myalgic syndrome of the aged, pseudo-polyarthrite rhizomelique, and anarthritic rheumatoid disease. It is likely that many such reports were not of polymyalgia rheumatica but of similar but non-specific aches and pains.

Senile rheumatic gout

A condition described as senile rheumatic gout, “a distinct form of disease,” by Bruce in 1888³ is often referred to as the first account of PMR, though reading his cases, this is not wholly convincing. His patients were all men in their seventies save for one aged sixty. He contended:

In the majority of cases a distinct history of gout can be made out… These acute senile cases belong to a different category from gout and rheumatism on the one hand and rheumatoid arthritis on the other.

However, he noted in his first case:

The whole aspect of his case leaned more to the side of polyarticular gout, and yet the obstinacy of the attack, his age and history point more to rheumatoid arthritis.

Several cases were of acute onset and the patients became bedfast or helpless from pain and stiffness of the joints. There was sparse description of constitutional or inflammatory symptoms or signs, and of course there were no ESR (erythrocyte sedimentation rate) or C-reactive protein tests for inflammation at that time. Bruce noted its remarkable severity and complete curability with time. He ingenuously concluded, “I feel that I have been scarcely able to prove my contention that these acute senile cases belong to a different category from gout and rheumatism on the one hand and rheumatoid arthritis on the other.”

Polymyalgia rheumatica

Many years later, Holst & Johansen in 1945 described “peri‑extraarticular rheumatism” in five unusually young women (aged 48–61) with pain in their shoulders, arms, hips, and systemic symptoms of low-grade fever and weight loss. They all had a raised ESR.⁴ In the same year, Meulengracht described two similar patients with “humeroscapular periarthrosis” with protracted fever, loss of weight, and marked increase in sedimentation reaction.⁵ Kersley reported “a myalgic syndrome of the elderly with systemic reaction” in thirteen patients of average age seventy-one, responsive to cortisone.⁶

Bagratuni distinguished it from rheumatoid arthritis, noting a syndrome of pain and stiffness in the shoulder and pelvic girdles in the elderly with high ESR and no evidence of arthritis.⁷ Polymyalgia rheumatica was the name suggested by Bagratuni and also by Barber, who in 1957 reported twelve patients with widespread muscular pains without arthritis accompanied by a high ESR and occasional pyrexia.⁸ He distinguished the condition from rheumatoid arthritis.

Polymyalgia rheumatica is now recognized as a common but often overlooked disorder of the elderly, women more than men. Muscle biopsies show no defining pathology. The site of inflammation is mainly in the synovium and extracapsular musculo-tendinous junctions of shoulders and pelvis, shown by MRI and by 18F‑fluorodeoxyglucose (FDG) uptake (an indicator of inflammation) in many patients with PMR and also in giant cell arteritis.⁹ In GCA, persistence of inflammation in medium and large vessels appears to depend on a small population of highly specialized T-cells, which survive in the tissue microenvironment. Symptoms of PMR and GCA abate very quickly with prednisolone, but a maintenance dose is often necessary for two or more years to prevent relapse,¹⁰ or the more serious complications (such as blindness) of giant cell arteritis.

Giant cell arteritis

Alestig and Barr (1963) found changes of giant cell arteritis on temporal artery biopsy in seven out of ten patients with polymyalgia symptoms.² Subsequently, giant cell arteritis was shown in 10 of 29 patients with PMR.¹¹ And half the patients with temporal arteritis have symptoms of polymyalgia rheumatica.¹²

Jonathan Hutchinson, like Hughlings Jackson, trained as a medical student in the old York Medical School. Few doctors have been as versatile. He practiced at the London Hospital as surgeon, ophthalmologist, neurologist, and dermatologist. In 1890, he described the first clear instance of temporal arteritis:

The subject…was an old man…the father of a well remembered beadle at the London Hospital College 30 years ago…I was asked to see him because he had ‘red streaks on his head’ which were painful and prevented his wearing his hat. The ‘red streaks’ proved to be his temporal arteries which…were inflamed and swollen. Pulsation could be feebly detected in the affected vessel, but it finally ceased; the redness then subsided, and the vessels were left impervious cords. The old gentleman lived, I believe, several years after this without any other manifestation of arterial disease.¹³

Although headache does not figure prominently in Hutchinson’s description, the inflammatory signs are unmistakable.¹⁴ Widespread recognition succeeded the seminal 1932 paper of Horton, Magath and Brown: “An undescribed form of arteritis of the temporal vessels demonstrating the histology,” though undescribed it was not. They presented two patients with headache, scalp tenderness, and constitutional symptoms; temporal artery biopsies showed granulomatous “temporal arteritis.”¹⁵ In a 1957 letter to the Mayo Clinic Board of Governors, Horton related his visit on 11 April 1931:

As I entered her room on the morning of April 11th, the light from the window, falling across the left side of her face and head, clearly outlined the enlarged red and somewhat nodular left temporal artery. I had the artist make a sketch of the left side of the head. Later that day, I persuaded one of the surgical first assistants to resect the temporal artery.

This showed a granulomatous arteritis, which he thought was a form of periarteritis. He later wrote:

About 5 weeks later, while … talking with the late Dr George Brown, a bald headed man came walking down the corridor toward us. I was discussing the case of [the first patient] with Doctor Brown as the [male] patient approached us. Doctor Brown looked up and said, “If she represents a new disease, here is a second patient with the same illness.” That proved to be true.

Gilmour in 1941 showed multinucleated giant cells in temporal arteritis, and in the aorta and its branches.¹⁶ Cooke et al. (1946) also emphasized a widespread but rarely recognized arterial disease.¹⁷ CV Harrison provided an early comprehensive review of the nomenclature, pathology, and clinical features.¹⁸ In GCA, dendritic cells in the adventitia and macrophages recruit and activate T-cells causing vascular pro-inflammatory cytokines.

PMA and GCA are closely linked clinical disorders. But it is not universally accepted that PMR is simply a variant of GCA.

References

1. Paulley JW, Hughes J P. Giant-cell arteritis, or arteritis of the aged. British Medical Journal 1960;2(5212)1562–1567.
2. Alestig K, Barr J. Giant-cell arteritis. A biopsy study of polymyalgia rheumatica, including one case of Takayasu’s disease. Lancet 1963;1:1228–30.
3. Bruce W. senile rheumatic gout. British Medical Journal 1888;2:811-13. https://pmc.ncbi.nlm.nih.gov/articles/PMC2198572/pdf/brmedj04695-0009.pdf
4. Holst, JE, Johansen, E. A special type of rheumatic disease. Acta Med Scand 1945;122:258-270.
5. Meulengracht, E. Schwartz M. Humeroscapular periarthrosis with protracted fever, loss of weight and marked increase in sedimentation reaction; 2 cases. Nord Med 1945;27:1569.
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14. Pearce JMS. Sir Jonathan Hutchinson (1828–1913) An early description of Temporal arteritis. J Neurology Neurosurgery Psychiatry 1994;57:216.
15. Horton BT, Magath TB, Brown GE. An undescribed form of arteritis of the temporal vessels. Proc Staff Meet Mayo Clin 7, 1932; 700–1.
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