Birth history of the child was normal, with normal APGAR score

Birth history of the child was normal, with normal APGAR score. confirmed the presence of NMDAR (N-methyl-D-aspartate receptor) antibodies in all the 12 young women. Anti-NMDAR encephalitis was initially classified as a paraneoplastic syndrome (up to 60% of them are associated with a teratoma or other tumor type), but it is now classified more as an immune-mediated encephalitis.3,4Moreover, since the first clinical descriptions, other cases have been reported in women without teratoma, but also in males and children. 5Only a few cases of anti-NMDAR encephalitis were reported to have occurred during pregnancy or postpartum. We report a case diagnosed in the first trimester of pregnancy. == CASE REPORT == This 21-year-old Caucasian woman developed behavioral changes during the 10th week of pregnancy. She had no medical past history and was first admitted to the Department of Psychiatry for a presumptive depression, she was treated with fluoxetine (and tiapride for agitation), without any improvement. After a few days, because of a worsening of her mental status and then muteness, she was finally admitted to the Department of Neurology where she FM19G11 presented a first generalized seizure. At that time, the clinical examination showed orofacial and limb dyskinesia, but no pyramidal sign, no motor weakness, no sensory disturbance, no autonomic disturbance, and no abnormality of the cranial nerves; deep tendon reflexes were normal; the body temperature was normal (37.2C) as well, and we observed no neck stiffness. The first brain MRI (magnetic resonance imaging) was unremarkable. The electroencephalogram showed a generalized slow theta activity without epileptic discharges; anticonvulsivant treatments (clonazepam and FM19G11 lamotrigine) were begun. Results of the cerebrospinal fluid (CSF) analysis showed a lymphocytic pleiocytosis (120 white cells/mm3), a moderate increase of the protein level (67 mg/dL; normal value < 45 mg/dL), and a normal glucose level (59 mg/dL). A treatment with acyclovir was started for a presumptive viral encephalitis (also with ampicillin for a few days) but was finally stopped because of the negativity of the polymerase chain reaction herpes simplex and varicella-zoster viruses in the CSF (and the absence of other germs). Other serologies (Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus,Borrelia burgdorferi,Leptospira,Coxiella burneti, andMycoplasma pneumonia) were negative. Other ancillary tests, comprising immunological tests (antinuclear and anti-desoxyribonucleic acid antibodies), were unremarkable; finally, NMDAR antibodies were identified in the CSF 20 days after the first neurological symptoms. An MRI of the abdomen and the pelvis was performed but showed no teratoma or other lesion. She was treated with methylpredinsolone (3 days, 250 mg/day), without improvement; then, a first course of intravenous immunoglobulins (IVIg) was performed during 5 days (20 g/day), but the patient still presented behavioral disturbances (alternating Mouse Monoclonal to Goat IgG episodes of catatonia and agitation) and visual hallucinations. One week later, because of a recurrence of seizures, she was admitted in the intensive care unit where she developed a status epilepticus, she gradually lost consciousness, experienced respiratory failure, and was intubated; the symptoms where difficult to control despite treatment with phenytoine, fosphenytoine, and propofol. A second brain MRI showed a diffuse meningeal enhancement (gadolinium) without other lesion, but it was performed only 24 hours after a second lumbar puncture. Two weeks after the first course of IVIg, she FM19G11 received a second course of IVIg (at the same dose). We progressively observed a gradual improvement for the next weeks, but with sequelae: 24 weeks after the onset of the disease, she.