Abstract
Neurologists are often called to evaluate central nervous system [CNS] manifestations in patients with suspected or definite systemic lupus erythematosus [SLE]. The manifestations are highly diverse and often have major prognostic consequences. The major difficulties are to determine if the given manifestation is primarily due to SLE activity in the brain, or a consequence of metabolic disturbances, infection, or corticosteroid use. The true incidence of CNS manifestations attributable to SLE is not entirely clear, but several studies show prevalence rate between 15-75%, depending on criteria adopted. For cognitive impairment, the prevalence ranges from 17-59%. Cognitive impairment may be attributed to emotional distress, corticosteroid use, active systemic disease or primary CNS dysfunction. These manifestations may occur even in the absence of other neuropsychiatric [NP] manifestations clearly attributable to SLE. The etiology of cognitive impairment may be related to autoimmune mechanisms, such as brain-specific autoantibodies. Despite several studies using computer tomography [CT] and magnetic resonance imaging [MRI], brain structural abnormalities could not be associated with cognitive findings in SLE patients. Functional neuroimaging methods may be more sensitive for detecting subclinical brain involvement related to cognitive dysfunction in SLE. Despite the fact that cognitive impairment may be residual in patients with previous CNS involvement, it also may be an early marker of CNS involvement in previous asymptomatic patients. This article will review clinical assessment, pathogenic mechanism, and the role of neuroimaging methods in the evaluating of SLE patients with cognitive impairment.
Keywords: Cognitive impairment, autoantibodies, brain imaging
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