Cerebral MRI abnormalities and their association with neuropsychiatric manifestations in SLE:: a population-based study

Objective: To evaluate the volumetric brain magnetic resonance imaging (MRI) findings in a population-based sample of systemic lupus erythematosus (SLE) patients and to detect a possible relationship between cerebral MRI abnormalities and specific neuropsychiatric (NP) manifestations. Methods: The study population consisted of patients with SLE (n=43) in Pirkanmaa Health Care District, Finland and of a sex- and age-stratified reference group from the general population (n=43). In addition to a clinical neurological investigation, all subjects received a detailed neuropsychological assessment and an MRI study. Volumetric measures of cerebral atrophy as well as T1- and T2-weighted lesions were obtained. SLE activity was assessed by the European Consensus Lupus Activity Measure (ECLAM) index, and accumulated NP abnormalities were measured by the Systemic Lupus International Collaborating Clinics (SLICC) damage index. A cumulative lifetime dose of glucocorticoids was determined from the patient records. Results: Compared with controls, SLE patients had increased volumes of both T1- and T2-weighted lesions (p=0.019 and p<0.0001, respectively) and increased cerebral atrophy (p<0.001). All the measured MRI parameters were statistically significantly higher in NPSLE than in non-NPSLE patients. In SLE patients, cerebral atrophy was associated with cognitive dysfunction, epileptic seizures, and cerebrovascular disease; T1- weighted lesions were associated with epileptic seizures and T2-weighted lesions with cognitive dysfunction. All MRI parameters correlated significantly with the SLICC index but not with the ECLAM index. A positive correlation was found between a cumulative dose of glucocorticoids and cerebral atrophy in SLE patients. Conclusion: MRI abnormalities, including brain atrophy and T1- and T2-weighted lesions, are significantly more common in patients with SLE than in the general population and they are related to specific NP manifestations. Our findings also provide support for the organic aetiology of cognitive dysfunction in SLE.