Abstract
Introduction
CNS lupus (also referred to as neuropsychiatric lupus erythematous)1 with diffuse manifestation appears to be primarily caused by autoantibodies directed to neuronal cells or their products. These autoantibodies are hypothesized to affect neuronal function in a generalized manner. Studies suggest that increased levels of inflammatory cytokines, induction of nitric oxide production, oxidative stress, and excitatory amino acid toxicity also may contribute to diffuse CNS dysfunction in SLE. Patients with acute encephalopathy frequently demonstrate elevated levels of antineuronal antibodies or other evidence of autoantibody production in the cerebrospinal fluid. As in multiple sclerosis, elevated levels of IgG and oligoclonal bands are markers of abnormal autoantibody production within the CNS and are frequently present in CNS lupus with diffuse manifestations. In patients with diffuse CNS lupus who present with primarily psychiatric disease, serum antiribosomal P antibodies appear to be a helpful diagnostic marker.
CNS lupus with focal manifestations is most likely to be related to intravascular occlusion. Magnetic resonance imaging (MRI), which is much sensitive than computed tomography (CT) scanning, almost always shows abnormalities characteristics of ischemic damage in these patients. Furthermore, these patients frequently demonstrate significantly elevated serum levels of antiphospholipid antibodies, which are associated with intravascular occlusion. Less commonly, evidence of vasculitis is apparent.
This study aims to study the cognitive dysfunction and seizure in SLE.
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Corresponding Author
Dr. Suresh Raghavan
Professor, Department of Medicine, Government Medical College, Kottayam,
Medical College Road, Gandhi Nagar, Kottayam, Kerala 686008, India
DOI: https://dx.doi.org/10.18535/jmscr/v9i7.20
