Acute manic state with psychotic features in a teenager with autoimmune encephalitis: a case report.

INTRODUCTION: Autoimmune disorders have become increasingly acknowledged as having a more causative role in encephalitis than previously assumed. Anti-N-methyl-D-aspartate receptor encephalitis seems to be the most prevalent disorder. Symptoms of the neuropsychiatric phase in children and adolescents include abnormal behavior, seizures, and neurologic symptoms. We present a report on a teenage girl with predominantly psychiatric symptoms, highlighting the need for awareness of the disease and multidisciplinary collaboration. CASE PRESENTATION: Our patient, a 17-year-old girl of Middle Eastern origin, had no earlier medical history, but a family history of autoimmune disease. One morning, she could not recognize her mother and soon developed increased energy and pressured speech. The condition worsened, with paranoid delusions. In the emergency unit, she ran around speaking incoherently. The condition was interpreted as a full-scale mania. After pediatric clearance, the patient was admitted to the Department of Child and Adolescent Psychiatry. Mood-stabilizing treatment was initiated with second-generation psychotics and lithium, but this brought no improvement. A multidisciplinary discussion was held with physicians from psychiatry and neurology. A lumbar puncture showed N-methyl-D-aspartate receptor antibodies, and autoimmune treatment was initiated. Computed tomography thorax/abdomen revealed a right-sided ovarian tumor. After salpingo-oophorectomy, our patient's mental status gradually improved, as demonstrated by repeated testing. Seven months post discharge she was in a stable relationship and performing well in school. CONCLUSION: This case underlines the importance of collaboration between child and adolescent psychiatry and pediatrics, and gives pointers for timely diagnosis. Manic adolescents who do not respond to mood-stabilizing treatment should be subjected to further consultations and investigations. Psychiatrists and neurologists should develop an integrated approach to the management of brain disorders.

Are Perinatal Events Risk Factors for Childhood Thyroid Autoimmunity?

BACKGROUND: Environmental and genetic factors possibly trigger thyroid autoimmunity. Studies on perinatal risk factors for childhood thyroid autoimmunity are sparse. OBJECTIVES: The aim was to investigate if perinatal factors, family history of autoimmune diseases, and HLA-DQ genotypes contribute to thyroid autoimmunity in the Diabetes Prediction in Skåne (DiPiS) study. METHODS: Samples from 1,874 ten-year-old children were analyzed for autoantibodies to thyroid peroxidase (TPOAb), thyroglobulin (TGAb), and HLA-DQ genotypes. Information on perinatal events and family history of autoimmunity was gathered prospectively in questionnaires. RESULTS: Thyroid autoimmunity was found in 6.9% of the children (TPOAb 4.4%, TGAb 5.8%, both autoantibodies 3.3%) and was overrepresented in girls. Prematurity was positively related to TGAb (OR: 2.4, p = 0.003, pc = 0.021). Autoimmune diseases in the family increased the risk of thyroid autoimmunity: TPOAb (OR: 2.2, p = 0.012), any autoantibody (OR: 1.7, p = 0.04), and both autoantibodies (OR: 2.2, p = 0.024). A first-degree relative (FDR) with thyroid disease increased the risk for TPOAb (OR: 2.4, p = 0.03) and both autoantibodies (OR: 2.6, p = 0.03), a FDR or sibling with celiac disease increased the risk for both autoantibodies (OR: 3.7, p = 0.03, and OR: 4.8, p = 0.003), a FDR or sibling with diabetes increased the risk for thyroid autoantibody (OR: 3.0, p = 0.01, and OR: 5.4, p = 0.032), and a father with rheumatic disease increased the risk for TPOAb (OR: 15.2, p = 0.017), TGAb (OR: 11.3, p = 0.029), any autoantibody (OR: 9.6, p = 0.038), and both autoantibodies (OR: 20, p = 0.01). CONCLUSIONS: Thyroid autoimmunity was found in 6.9% of the 10-year-old children who were being followed for their risk of type 1 diabetes. No relation to perinatal factors was found, with the exception of a possible association between prematurity and TGAb. Family history of autoimmune diseases increased the risk of thyroid autoimmunity.