Incidence of temporal arteritis in patients with polymyalgia rheumatica: a prospective study using colour Doppler ultrasonography of the temporal arteries
W. A. Schmidt and
E. Gromnica-Ihle
Medical Centre for Rheumatology Berlin-Buch, Karower Strasse 11, 13125 Berlin, Germany
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Abstract
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Objective. To determine the incidence of temporal arteritis (TA) in patients with polymyalgia rheumatica (PMR) using colour Doppler ultrasonography of the temporal arteries.
Methods. Ultrasonography was performed in all 127 consecutive patients with newly diagnosed, active PMR seen between 1994 and 2000 and in 127 age- and sex-matched controls.
Results. Of 102 patients with pure PMR, 8% had ultrasonographic findings arousing suspicion of concomitant active TA (specific halo sign and/or positive histology in 7%; histologically proven TA in 4%). Twenty-five patients had clinical signs of both PMR and TA. Histology and sonography were negative in three of these patients. Of the controls, none had a halo sign and four had stenoses.
Conclusion. Ultrasonography of the temporal arteries is a new, non-invasive method of diagnosing concomitant TA in patients with PMR.
KEY WORDS: Temporal arteritis, Polymyalgia rheumatica, Ultrasonography, Colour Doppler ultrasonography, Temporal artery histology.
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Introduction
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The incidence of temporal arteritis (TA) in patients with polymyalgia rheumatica (PMR) is highly controversial. In patients without clinical signs of TA (pure PMR [1]) it ranges between 0% and 41% [212]. Most authors do not recommend temporal artery biopsy to be done routinely in patients with pure PMR [1]. As an alternative to histology, diagnosis of TA may be made by colour Doppler ultrasonography (US) of the temporal arteries. The sensitivity and specificity of this method are similar to those of histology [1315]. The aim of this study was to determine the incidence of TA in patients with the clinical diagnosis of PMR using colour Doppler US of the temporal arteries.
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Methods
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All consecutive patients with newly diagnosed, active PMR who were seen in a 7-yr period at the Medical Centre for Rheumatology in Berlin-Buch, Germany were investigated. Colour Doppler US of the temporal arteries was performed in all patients and in age- and sex-matched controls.
Patients
All 127 patients with newly diagnosed PMR seen between 1 January 1994 and 31 December 2000 were included in the study if they were untreated or had received corticosteroid treatment for <7 days. In an earlier study we found that inflammatory changes of the temporal arteries detected by US persisted for at least 6 days with treatment [13]. All patients fulfilled at least three of the seven criteria of the Bird classification for PMR: bilateral shoulder pain or stiffness, duration of illness <2 weeks, initial erythrocyte sedimentation rate (ESR)>40 mm/h, duration of morning stiffness >1 h, age
65 yr, depression and/or weight loss, and bilateral tenderness in the upper arms [16]. The diagnosis was established by at least two rheumatologists, who examined every patient.
Twenty-five patients had clinical signs of TA (new onset of localized headache, and/or hard, swollen temporal arteries, and/or temporal artery tenderness, and/or decreased temporal artery pulse, and/or jaw claudication) (group A). After the final diagnosis had been established, they fulfilled at least three of the ACR classification criteria for giant cell arteritis (GCA): age
50 yr, new onset of localized headache, temporal artery tenderness or decreased pulse, ESR
50 mm/h, and histological findings [17].
One hundred and two patients had pure PMR, i.e. they had clinical signs of PMR without features of TA, as mentioned above. Once US of the temporal arteries had been performed, the patients were classified into two groups: those with US findings arousing suspicion of active TA, i.e. the halo sign, stenosis, or occlusion of the temporal arteries (group B) and those with normal US findings (group C). Eight patients were classified in group B and 94 in group C.
One hundred and twenty-seven age- and sex-matched control subjects were investigated (group D). These persons had no history of TA or PMR and no previous temporal artery biopsy.
Table 1
provides further information on the patients and controls investigated.
Ultrasound examination
Simultaneous colour Doppler and duplex US was performed by an experienced physician (WAS) as described earlier [13, 14, 18]. The common superficial arteries were investigated, including the parietal and frontal ramus, as completely as possible on both sides before a biopsy was performed. The possible pathological findings were as follows.
Hypoechoic wall thickening (halo). A dark area is found around the perfused lumen, which looks like a halo in the transverse plane (
Fig. 1). This finding is due to oedema. It is a specific sign of TA in our experience. This finding has to be demonstrated in two planes. The halo is usually circumferential. It disappears within 16 days (756 days) with corticosteroid treatment [13]. Coloured images of this phenomenon can also be found in earlier publications [13, 14, 18, 19].

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FIG. 1. Right superficial common temporal artery in a transverse plane. The hypoechoic (black) area around the perfused lumen is considered to be an oedematous wall thickening due to TA. The numbers at the right indicate millimetres below the skin surface. The triangle indicates the point of focus.
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Occlusion. When there is an occlusion in a temporal artery, conventional grey-scale US reveals the wall of the artery with a dark area in the centre. Colour Doppler US fails to show a colour signal in this dark area, i.e. no blood flow can be demonstrated (
Fig. 2). Occlusion of a temporal artery is thus distinguished from aplasia, in which no vessel at all can be detected by US.

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FIG. 2. Occluded distal frontal ramus of the right superficial temporal artery. No perfusion can be seen in the central dark area. The numbers at the right indicate millimetres below the skin surface.
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Stenosis. Stenoses are detected by colour Doppler US and confirmed by simultaneous pulsed-wave Doppler US. In the colour image, turbulent flow is seen combined with increased persistent flow during diastole. Stenosis is considered to be present if the blood-flow velocity is more than twice the rate recorded by pulsed-wave Doppler US in the area before the stenosis, perhaps with waveforms demonstrating turbulence (
Fig. 3).

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FIG. 3. Stenosis in the frontal ramus of the left superficial temporal artery. On the left, systolic and diastolic blood flow are increased as the pulsed-wave Doppler beam moves through the stenosis. In the area beyond the stenosis on the right, blood-flow velocity decreases. The numbers at the right indicate flow velocity in cm/s.
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All investigations were performed with a high-resolution scanner (ATL Ultramark 9 HDI; Advanced Technology Laboratories, Bothell, WA, USA) with a linear 10 to 5 MHz probe (L105, length of probe, 38 mm). The settings of the ultrasound equipment were as follows: dynamic range, 50 dB; signal processing characteristic, G6; dynamic contrast gain, K4; colour gain, 78%; type of colour gain, V; colour scale, 4; colour sensitivity, 10; colour wall filter, 100 Hz; colour persistence, 4; pulse repetition frequency, 2500/s; dynamic movement differentiation, D3; focus point position, 7 mm.
Temporal artery biopsy
Bilateral temporal artery biopsy was planned if clinical signs of concomitant TA were present, or if US findings suggested active TA due to hypoechoic wall thickening, stenosis, or occlusion of the temporal arteries. It was performed in all eight patients with pure PMR and pathological US findings (group B) and in 20 of the 25 patients with symptoms of both PMR and TA (group A). Five of these patients did not agree to be biopsied. Additionally, biopsy was performed in 11 patients with pure PMR and normal US findings (group C).
TA was diagnosed if histology demonstrated vasculitis of the temporal arteries with a predominance of mononuclear cell infiltration or granulomatous inflammation with or without giant cells [17].
Statistical analysis
The SPSS statistical package (SPSS Inc., Chicago, IL, USA) was used for statistical analysis. The MannWhitney U-test or the
2 test was used to compare the results between groups.
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Results
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The patients with clinical signs of both PMR and TA (group A) were slightly but not significantly older than the patients with clinically pure PMR (groups B and C). The ESR was significantly higher in the patients of group A (P<0.01). The clinical picture of PMR was the same in the three groups. Patients in groups A, B, and C had the same number of positive classification criteria for PMR. In the patients with clinically pure PMR who had pathological (group B) and normal (group C) US findings, there was no difference in age, number of PMR classification criteria and ESR (Table 1
).
In 22 of the 25 patients with clinical symptoms of PMR and TA (group A), US revealed a halo, a stenosis or an occlusion. The temporal arteries of three patients were normal in terms of US and histology: (i) an 82-yr-old female with new onset of headache, thickened, hard, but not tender temporal arteries with normal pulsation, no jaw claudication, ESR 80 mm/h and three positive ACR classification criteria for the diagnosis of TA; (ii) a 71-yr-old female with new onset of headache, clinically normal temporal arteries and no jaw claudication, ESR 80 mm/h and three positive ACR criteria; and (iii) a 52-yr-old female with new onset of headache, no palpable pulse of both frontal rami, no jaw claudication, ESR 96 mm/h and four positive ACR criteria. These patients were classified as histology- and US-negative TA and treated with corticosteroids, as were the other patients.
Four patients of group A with the US finding of temporal artery stenoses only and no signs of inflammatory wall thickening (halo) or occlusion also had pathological histological findings. Twenty patients of group A had headache, 17 had swollen and hard temporal arteries, 14 had tender temporal arteries, eight had a reduced pulse rate and 10 had jaw claudication.
In eight of the 102 patients with clinically pure PMR, US revealed a pathological finding, as shown in Table 1
(group B). These patients are described in more detail in Table 2
. In four of these patients, histology confirmed the diagnosis of TA suggested by US. In three of the four other patients, a halo was seen; this is taken as specific for TA in our experience [13, 14]. None of the controls (group D) had this hypoechoic wall thickening of the temporal arteries. The three patients of group B with a halo found in US and negative histological findings are described in more detail. (i) A 58-yr-old female had an 8-mm long area with a halo that had a diameter of 0.6 mm around the perfused lumen in the right superficial common temporal artery close to the bifurcation (Fig. 1
) and a short stenosis in this region. Additionally, a 2-cm long stenosis was detected in the proximal right common superficial temporal artery. (ii) A 64-yr-old male had a 4-mm long halo with a diameter of 1.0 mm in the left superficial common temporal artery and an occlusion of the distal right frontal ramus (Fig. 2
). (iii) An 84-yr-old male had a 10-mm long halo with a diameter of 0.4 mm at the proximal left frontal ramus with a short stenosis (Fig. 3
). Another short stenosis was found in the right distal frontal ramus.
These three patients had a halo in only one segment of the temporal arteries, whereas the three clinically pure PMR patients with a halo and positive histological findings had a halo in two, three and seven segments of their temporal arteries. We have defined four segments on each side of the head (common superficial temporal artery, parietal ramus, proximal frontal ramus and distal frontal ramus) [13]. The diameter of the halo was 0.5, 0.5 and 1.1 mm respectively in these three patients. In two of these patients the halo was bilateral.
In all three patients with a negative biopsy despite a halo, both distal frontal rami were biopsied. Thus, the biopsy could not be taken from a segment with a halo. The proximal frontal ramus cannot be biopsied because of the likelihood of facial nerve irritation. The common superficial temporal artery is not removed to prevent the possibility of ischaemia.
In 18 patients of group A, a halo was found. The number of segments involved was one in three patients, two in four patients, four in five patients, five in one patient, six in two patients, seven in one patient and eight in two patients. In 15 of these 18 patients, the halo was bilateral.
Another patient of group B had a pathological US finding and negative histological findings. This patient had a stenosis of the left common superficial temporal artery without any halo or occlusion. It remains open whether this finding was due to inflammation or arteriosclerosis, as stenoses were also found in 3% of the controls.
Ninety-four patients with clinically pure PMR (group C) had a normal US examination with the exception that at least one of the rami could not be detected in 4% of these patients. This was also the case in 5% of the controls, and was considered to represent aplasia of one of the branches.
In summary, 8% of the patients with clinically pure PMR had findings suggestive of TA by US of the temporal arteries, in 7% TA was highly probable because of specific US and/or histological findings, and in 4% it was proven histologically.
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Discussion
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Considerable overlap between PMR and TA exists. It is unclear whether a patient develops PMR or TA. This may depend on the cytokines that are activated. High levels of interleukin (IL)-2 are associated with PMR, whereas high levels of interferon
and IL-1ß mRNA have been detected in inflamed temporal arteries [20]. On the other hand, high levels of IL-6 are associated with the disease activity of both TA and PMR [21]. Also, increased uptake of fluorodeoxyglucose in the larger thoracic arteries, suggestive of vasculitis, was detected by positron emission tomography in most of the patients with TA and PMR but not in controls [22].
The results of studies investigating the incidence of PMR in patients with TA show good correspondence. Forty to fifty per cent of patients with TA have symptoms of PMR (Table 3
). This agrees with our own experience.
On the other hand, the incidence of TA in patients with PMR is a subject of controversy in the literature. Table 4
summarizes the results of studies with temporal artery biopsies done in patients with clinically pure PMR. Two studies did not report any positive histology, whereas there were positive histological findings in 41% of the patients in two other studies. It was suggested that the differences were due to the race of the patients investigated. Spiera and Davison did not find any GCA in a mainly Jewish population of New York city [3], whereas most of the early studies in which there was a high incidence of GCA came from Scandinavia [1012]. This theory can no longer be supported, as a study from Norway, published in 1996, showed an incidence of only 4% [4]. In a recent small study in the south-west of Germany, the incidence of TA in patients with clinically pure PMR was 21% according to histological findings and 32% according to colour Doppler US of the temporal arteries [9]. These incidences are much higher than those in our patients from north-east Germany, in whom the incidence is 4% by histology and 7% by US plus histology. The risk of an abnormal biopsy is increased in patients with the characteristic cranial manifestations of GCA, raised liver enzymes, ESR
100 mm/h, anaemia and age
70 yr [23]. One reason for the differences among these studies may be the definition of pure PMR. If all patients with PMR are investigated carefully, pathologies of the temporal arteries can be found even if there is no headache: swollen, hard or tender temporal arteries or decreased pulse. Of the five patients in our group A without headache, three had no pulse in a frontal ramus as the only sign of TA, one only had a hard, swollen frontal ramus and one had a hard, swollen and pulseless frontal ramus. The differences between the studies may also be due to differences in the way the patients were referred to the centres.
PMR manifestations may occur before or after the cranial manifestations of GCA [24, 25, 26, 27]. Peripheral arthritis occurs much more frequently in patients with PMR than in those with TA [28]. The health assessment questionnaire (HAQ), originally developed for patients with RA, is also useful in the assessment of the disease activity in PMR [29].
Colour Doppler US of the temporal arteries is a sensitive, non-invasive method of detecting active TA. An inflammatory wall thickening (halo) was seen in 71% of the patients with the clinical diagnosis of TA and in 80% of the patients with positive temporal artery histological findings. Stenoses or occlusions were found in 80 and 91% respectively. Overall, at least one of these features was found in 89% of the patients with the clinical diagnosis and in 97% of the patients with positive histological findings [14].
The sensitivity of temporal artery histology in the clinical diagnosis of TA has been reported as being between 56 and 91% (Table 5
). US and histology evaluate different aspects of the disease: vessel wall oedema, stenoses and occlusions vs cell infiltrates. The total length of the superficial temporal arteries can be evaluated by US, whereas histology can give a false-negative result because of skip lesions. These skip lesions can be seen frequently by US, as mentioned above. We believe that the three patients with clinically pure PMR who had US (halo) and negative histological findings had concomitant TA. To date we have seen three additional patients outside this study with typical clinical signs of TA and a halo but negative histological findings. Two of these patients have been described earlier [13]. We did not find the halo in any of the controls or in any other patient outside this study without TA or PMR. Since the end of 1993, we have investigated more than 600 persons with this method.
Stenoses are found in most patients with active TA, but this finding is not completely specific. They also occur in about 3% of persons with other diseases due to arteriosclerosis, as confirmed in this study.
In our study, biopsy was performed in 11 of the 94 patients with clinically pure PMR and normal US findings. Histology was negative in all of these patients. Nevertheless, we cannot exclude the possibility that US may have missed concomitant TA in some of the other patients without biopsy.
In some patients, no parietal or frontal ramus had been detected by US. This is consistent with a post-mortem study that found only one terminal branch of the superficial temporal artery in 3% of the subjects as an anatomical variant [30].
With respect to the clinical diagnoses, bias may have resulted from the fact that those who made the final diagnosis were in many cases aware of the results of the US investigations.
In a few cases, TA is due to a form of vasculitis other than GCA. One case with a temporal artery halo seen by US and the histological diagnosis of polyarteritis nodosa has been described [31]. Other vasculitides, such as Wegener's granulomatosis, can also involve the temporal arteries, or even the carotid arteries [32]. On the other hand, larger arteries can be affected in TA, such as the axillary and brachial arteries (large-vessel GCA). The US image of these arteries is similar to that described in cranial TA [33].
Neither US nor histology will be able to determine the true number of PMR patients with concomitant TA. In particular, some patients with PMR may have only a small amount of inflammation of the temporal arteries, which may be missed by both US and histology. Nevertheless, diagnostic sensitivity may be improved if US and histology are combined, and in some patients without clinical signs of cranial arteritis GCA may be detected non-invasively by US. Thus, the temporal arteries of the patients with clinically pure PMR may be investigated non-invasively by US. When there are pathological findings, such as a halo around the perfused lumen, a stenosis or an occlusion of the temporal arteries, biopsy can be performed to confirm the diagnosis of GCA.
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Notes
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Correspondence to: W. A. Schmidt. 
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Submitted 30 January 2001;
Accepted 6 July 2001