Case presentation 
Sixteen years old female was referred to rheumatology with a history of progressive forgetfulness and episodes of jerky movements that were associated with loss of consciousness, upward rotation of both eyeballs, tongue bite, and frothy secretions from the mouth, which persisted for 3 to 10 minutes and followed by an incoherent talk. She had complained of a headache for the last 12 months. There was no history of cough, vomiting, blurred vision, head injury, anorexia, weight loss, or travel history to a malaria area. She is nonsmoker nor an alcoholic. She is allergic to penicillin. Her family history of autoimmune diseases and encephalitis is unremarkable. She was seen in ER in another hospital and then was labeled as a case of suspected viral encephalitis associated with fever; a lumbar puncture was done, then started on antiviral for 14 days and discharged. After that, she still noticed behavioral changes like depression, increased forgetfulness, and recurrent attacks of seizures with agitation for one month. Later on, she presented to our clinic and was diagnosed to have systemic lupus erythematosus based on her clinical presentation, which included neurological manifestations and malar rash, and lab results which showed positive ANA and dsDNA.On initial examination, the patient was found agitated but oriented. Her vital signs were, her pulse rate was 87 beats/minute, her blood pressure was 166/91 mm Hg, her Respiratory rate was 17/minute, her temperature: was 36°C, and her weight was: 102 Kg. She had a photosensitive malar rash, alopecia, lymphadenopathy, and thyroid nodules. Other neurological examination findings were normal, and examination of other systems also revealed no other abnormalities.Investigations done were , complete blood count (CBC) showed decrease in white blood cells (WBC) = 2700 /μL (4.1 – 11.6 ), increase in monocytes = 14.4% (3.8 – 11.2), normal red blood cells (RBCs) count, and normal hemoglobin (HGB) level. The liver function tests (LFT) showed mild elevation of alanine aminotransferase (ALT) = 44 (0 – 40), normal albumin level, and other findings were normal. Kidney function test (KFT) showed creatinine level = 33 μmol/L (44 – 80), urea level = 1.95mmol/L (2.1 – 7.1), and other findings were normal. Urine analysis showed negative blood, negative protein, negative glucose, and other findings were normal. Erythrocyte sedimentation rate (ESR) was 07 mm/hour (0 – 20). C-reactive protein (CRP) was positive, and rheumatoid factor (RF) and Anti-cyclic citrullinated peptide (ANTI-CCP) were negative. Anti-dsDNA antibodies was positive 81.7 IU/mL (positive > 35). C3 complement was 90 mg/dL (90 – 180) and C4 complement was 12 mg/dL (12 – 40). A thyroid function test (TFT) revealed a mild decrease in free thyroid hormone 3 (FT3) with normal thyroid-stimulating hormone (TSH) and free thyroid hormone 4 (TF4) levels. ECG shows sinus tachycardia. EEG was done and showed normal brain activity. MRI for the brain revealed prominent sulci, mainly Sylvian fissure, corpus callosum atrophy, and bilaterally prominent temporal horns with relatively symmetrical increased FLAIR signal intensity of both hippocampal formations (figures 1a, 1b, 1c, and 1d ). Ultrasound for thyroid shows multiple bilateral nodules with tiny calcific foci. An echocardiogram revealed trace aortic and mitral regurgitation, impaired relaxation by tissue Doppler, no pericardial effusion, and normal ventricular dimension. CT of the chest, abdomen, and pelvis was done, and their results were unremarkable.