Cognitive Dysfunction in Neuropsychiatric Systemic Lupus Erythematosus

Melanie J. Harrison, MD, MS, Lisa D. Ravdin, PhD

Disclosures

Curr Opin Rheumatol. 2002;14(5) 

In This Article

Introduction

Neuropsychiatric syndromes associated with systemic lupus erythematosus are common, but diverse in etiology and presentation. Cognitive dysfunction is prevalent among these syndromes, but exhibit a significant degree of heterogeneity both within and between patient variability. Earlier studies of SLE-associated cognitive dysfunction addressed its identification and description. Common associations were repeatedly acknowledged, including concomitant or past neuropsychiatric disease, use of corticosteroids, disease activity, emotional disturbance, and antiphospholipid antibodies. The past several years have focused more on elucidating the relative strengths of various risk associations, patterns of cognitive abnormalities, both cross-sectionally and longitudinally (ie, clinical course), and novel means to identify cognitive impairment, both functionally and biologically.

Cognition is the sum of intellectual functions that result in thought. The functions include reception of external stimuli, information processing, learning, and expression. Cognitive functioning can be conceptualized as consisting of domains or categories, each of which involves a variety of cognitive processes, such as complex attention, verbal memory, perceptual skills, reasoning and judgment, insight, and awareness. Disruption of any individual function leading to the production of normal thought within any domain can be considered cognitive dysfunction. Depending on the nature and extent of the etiologic insult, cognitive dysfunction may be limited to a particular domain, or may be so extensive that global impairment results.

Since the first publication by Carbotte et al. in 1986,[1] it has become widely accepted that cognitive dysfunction is prevalent among patients with systemic lupus erythematosus (SLE). Despite the increased awareness among clinical rheumatologists and researchers, the etiology, nature, course, and treatment for SLE-associated cognitive dysfunction remain elusive.

Cognitive dysfunction is prevalent in SLE, with wide-ranging estimates varying from 12 to 87%.[1,2,3,4,5,6,7,8,9,10] This variability is not surprising, given the diversity of demographic and SLE disease characteristics; the variety of neuropsychological tests employed, and the diversity of outcome definitions of cognitive impairment, all of which contribute to the complexity of developing clear understanding of this condition. The evolution of our knowledge of SLE-associated cognitive dysfunction is not unlike that of conditions such as hypertension, HIV disease, or multiple sclerosis that diffusely affect the central nervous system (CNS). Initial studies were cross-sectional in design, employed a variety of selected neuropsychological tests, and often reported fairly high prevalence rates of abnormal cognitive performance. Upon further study, other investigators report conflicting results with regard to prevalence rates and risk factor associations. These follow-up studies are not easily comparable because of differences in patient populations, neuropsychological test batteries, decision rules for the classification of cognitive abnormality, and control populations.

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