Systemic lupus erythematosus (SLE) is a chronic autoimmune disease involving multiple organs, characterized by the production of autoantibodies and the development of tissue injury. The etiology of SLE is partially known, involving multiple genetic and environmental factors. As many as 50% of patients with SLE have neurological involvement during the course of their disease. Approximately 40% of neuropsychiatric SLE (NPSLE) cases are a consequence of the disease itself; other causes of NPSLE are infections, metabolic disorders, and side effects of drugs. The American College of Rheumatology identified 19 neuropsychiatric syndromes in SLE patients that can be divided into central and peripheral nervous system manifestations. Although this classification includes syndromes with no clear pathophysiological mechanism and is not specific for neuropsychiatric events caused exclusively by SLE, it helps the physician to recognize any neurological involvement . The most common clinical manifestations of juvenile neuropsychiatric SLE (NPSLE) are headache, cognitive dysfunction, mood disturbances and seizures. The pathophysiology of juvenile NPSLE is not yet fully known, but immunological and inflammatory factors, such as autoantibodies, cytokine and prothrombotic states are widely described . The of autoantibodies in the onset of specific clinical manifestations has also been recognized. Juvenile NPSLE manifestations are often difficult to diagnose (. Nineteen neuropsychiatric syndromes have been identified associated with SLE, can be divided into central and peripheral manifestations.