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Neurocognitive impairment in corticosteroid-naive patients with active systemic lupus erythematosus: a prospective
Katsuji Nishimura1, Masako Omori2, Yasuhiro Katsumata2
1From the Department of Psychiatry and Institute of Rheumatology, Tokyo Women's Medical University School of Medicine, Tokyo; Kanagawa Psychiatric Center, Yokohama; Department of Pharmacovigilance, Graduate School, Tokyo Medical and Dental University; Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.K. Nishimura, MD, PhD; J. Ishigooka, MD, PhD, Department of Psychiatry, Tokyo Women's Medical University School of Medicine; M. Omori, MD, Kanagawa Psychiatric Center; Y. Katsumata, MD, PhD; E. Sato, MD; T. Gono, MD, PhD; Y. Kawaguchi, MD, PhD; H. Yamanaka, MD, PhD, Institute of Rheumatology, Tokyo Women's Medical University; M. Harigai, MD, PhD, Department of Pharmacovigilance, Graduate School, Tokyo Medical and Dental University; M. Mimura, MD, PhD, Department of Neuropsychiatry, Keio University School of Medicine. nishimura.katsuji@twmu.ac.jp.
Objective:
Neurocognitive impairment (NCI) has been intensively studied in patients with systemic lupus erythematosus (SLE). However, those studies have mostly included patients who were treated with corticosteroids, which may itself induce NCI. We investigated NCI in corticosteroid-naive people with SLE who did not exhibit any overt neuropsychiatric manifestations.
Methods:
Forty-three inpatients with SLE who had no current or past neuropsychiatric history participated in the study. Patients and 30 healthy control subjects with similar demographic characteristics were given a 1-h battery of neuropsychological tests. NCI was defined as scores at least 2 SD below the mean of the healthy control group on at least 2 of the 7 neurocognitive domains. Results of clinical, laboratory, and neurologic tests were compared regarding the presence of NCI.
Results:
NCI was identified in 12 patients (27.9%) with SLE and in 2 control subjects (6.7%). Patients with SLE showed a significant impairment compared with controls on tasks assessing immediate recall, complex attention/executive function, and psychomotor speed. We identified psychomotor speed (Digit Symbol Substitution Test) as the factor that best differentiated the 2 groups. Further, we identified the score of the SLE Disease Activity Index 2000 as an independent risk factor for NCI in patients with SLE.
Conclusion:
We conclude that reduced psychomotor speed is an SLE-specific pattern of NCI. Verbal-memory deficits that have been reported in patients with SLE were not evident among patients who were corticosteroid-naive. Our results indicate that impaired psychomotor speed may be added to the symptoms of early SLE.
