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Quantitative cerebral MR in rheumatoid arthritis
S I Bekkelund1, C Pierre-Jerome, G Husby
1Department of Neurology, University of Tromsø, Norway.
Purpose:
To determine the presence of hyperintense white matter lesions and atrophy reflecting cerebral vasculitis in rheumatoid arthritis.
Methods:
Thirty-three patients with rheumatoid arthritis and 48 control subjects were examined with MR. Mean age was 45.1 years (range, 26 to 55 years) for the patients and 42.2 years (range, 25 to 55 years) in the control group. To determine atrophy we measured the area of corpus callosum, the cerebrum, and the cerebellum on midline sagittal sections. On transverse images, the ventricle-to-brain ratio, the bifrontal ratio, and the bicaudate ratio were selected as atrophy parameters. Area and signal intensity were measured for the biggest and the smallest lesions in both groups.
Results:
Nine patients (27%) had hyperintense lesions compared with 15 (31%) of the control subjects. Mean numbers of hyperintense lesions were 1.3 in patients and 2.1 in control subjects. Mean area of the largest lesion in each patient was 27.4 mm2 for the patients and 29.8 mm2 in the control group. In patients with long disease duration (> 15 years) the mean ventricle-to-brain ratio was 0.09 compared with 0.08 in the control subjects. The midsagittal area of the cerebellum was 1349.8 mm2 in the patients with long disease duration and 1573.3 mm2 in the control group. No difference in number of hyperintense white matter lesions was detected between patients with long disease duration and the control subjects. Comparing the total group of patients with the control subjects, no significant differences in atrophy parameters or hyperintense white matter lesions were found. Also, there were no significant differences in relative signal intensity of the hyperintense lesions and corpus callosum between the two groups. We were not able to detect differences between treated versus untreated patients.
Conclusion:
This study indicates a tendency of more cerebral and cerebellar atrophy in patients with severe rheumatoid arthritis. The number and size of the white matter lesions were not significantly different in the two groups and do not support a higher frequency of even clinically silent infarcts caused by vasculitis in the patients with rheumatoid arthritis compared with control subjects.
Insights
Rheumatoid arthritis patients show a tendency for cerebral and cerebellar atrophy, but not significantly more white matter lesions than controls. This suggests vasculitis is not a frequent cause of silent infarcts in rheumatoid arthritis.
Area of Science:
- Neurology
- Rheumatology
- Radiology
Background:
- Rheumatoid arthritis (RA) is a systemic autoimmune disease.
- Cerebral vasculitis can occur in RA, potentially leading to neurological complications.
- Magnetic resonance (MR) imaging can detect white matter lesions and atrophy.
Purpose of the Study:
- To investigate the presence of white matter lesions and atrophy indicative of cerebral vasculitis in rheumatoid arthritis patients.
- To compare MR imaging findings between RA patients and healthy controls.
Main Methods:
- MR imaging was performed on 33 RA patients and 48 controls (ages 25-55).
- Atrophy was assessed by measuring the corpus callosum, cerebrum, and cerebellum areas, and calculating ventricle-to-brain, bifrontal, and bicaudate ratios.
- Hyperintense white matter lesions were quantified by number, area, and signal intensity.
Main Results:
- No significant differences in the number or size of white matter lesions were found between RA patients and controls.
- A tendency towards increased cerebral and cerebellar atrophy was observed in RA patients, particularly those with long disease duration (>15 years).
- No differences were detected between treated and untreated RA patients, or in lesion signal intensity.
Conclusions:
- While RA patients may exhibit a trend towards cerebral and cerebellar atrophy, the study did not find evidence of increased white matter lesions.
- The findings do not support a higher frequency of clinically silent infarcts due to vasculitis in RA patients compared to controls.