Therefore, we considered that this seizures were associated with MOG positivity. Methylprednisolone pulse therapy and immunoglobulin immunomodulatory therapy are efficient first-line treatments for MOGAD, especially in the acute phase (17). and intravenous immunoglobulin (1?g/kg/day, administered for 2 consecutive days). 2.4. Statistical analysis Data were analyzed using SPSS 20.0 software both before and after the stratification of different clinical phenotypes and treatments. The normality of the data distribution was tested using the KolmogorovCSmirnov test. Continuous variables with a normal distribution were compared using the Students IgM antibody (Table 1). The pathogen detection rate in this cohort was 36.5%. Of the three patients with EBV seropositivity, one exhibited fever but showed no indicators of enlarged lymph nodes in the neck, enlarged liver or spleen, or abnormal liver function. There were also no abnormalities in the lymphocyte ratio and lymphocyte morphology. The other two patients did not present with any of these conditions. Table 1 Laboratory examination results of patients with different clinical phenotypes of MOGAD.
Mean leukocyte count (106?L)54.690.515.835.1175.7205563.3Mean protein concentration (mg/L)286241.9193.1290.8502.1280465.8295.8EBV-positive in CSF (n of patients who tested positive/total n of patients tested)1/27 (3.7%)1/10 (10.0%)0/60/71/5 (20.0%)0/00/03/55 (5.5%)HSV-positive in CSF (n of patients who tested positive/total n of patients tested)0/241/10 (10.0%)0/60/70/50/00/01/52 (1.9%)EBV IgM-positive (n of patients who tested positive/total n of patients tested)3/26 (11.5%)3/10 (30.0%)1/9 (11.1%)1/8 (12.5%)1/5 (20.0%)0/10/19/60 (15.0%)MP IgM-positive (n of patients who tested positive/total n of patients tested)7/25 (28.0%)1/10 (10.0%)4/9 (44.4%)1/8 (12.5%)1/5 (20.0%)0/00/114/58 (24.1%) Open in a separate windows MOGAD, myelin oligodendrocyte glycoprotein antibody-associated disease; ADEM, acute disseminated encephalomyelitis; ON, optic neuritis; NMOSD, neuromyelitis optica spectrum disorder; TM, transverse myelitis; CSF, Cerebrospinal fluid; EBV, EpsteinCBarr computer virus; HSV, herpes simplex virus; MP, mycoplasma pneumoniae. 3.3. Imaging characteristics All patients underwent MRI scans of the brain and spine. In addition to common imaging manifestations of ADEM, NMOSD, ON, and TM, one patient with NMOSD presented with area postrema syndrome (Physique 4). Of three children who presented with encephalitis but exhibited no significant abnormalities on cranial MRI in the early stage of the disease, two showed thalamic lesions at 2?weeks after onset, while one exhibited no abnormalities throughout the disease course. One patient who had meningitis and presented with fever as the only clinical manifestation at admission exhibited meningeal enhancement on Rabbit polyclonal to AP1S1 repeated cranial MRI (Physique 5). Open in a separate window Physique 4 Cranial MRI results of the patient with area postrema syndrome. A female child, aged 133?months, presented with bouts of vomiting CETP-IN-3 and dizziness for over 10?days. (A) Cranial MRI scan at admission. (A-a) Abnormal signal in the right side of the medulla oblongata in the FLAIR sequence. (A-b) Abnormal signal in the bilateral periventricular white CETP-IN-3 matter in the FLAIR sequence. (A-c) Patchy abnormal signal at the T11 level in the FLAIR sequence. (B) Cranial MRI at 30?months after the first MRI scan. The patient complained about headache and had vomited for 2?days. (B-a) The periventricular semioval center of the lateral ventricle in the FLAIR sequence. (B-b) The right medulla oblongata and periventricular white matter in the coronal section of the FLAIR sequence. (B-c) Abnormal signal in the dorsal side of the medulla oblongata in the FLAIR sequence. Open in a separate window.