ABSTRACT
Objective To summarize and analysis the clinical features, diagnosis and treatment of the cases which were positive for anti-N-methyl-D-aspartic acid (NMDA) receptor antibodies by indirect immunofluorescence assay (IFA). Methods We analyzed the disease process, clinical characteristics, auxiliary examination , diagnosis, treat-ment, and prognosis of five cases positive for anti NMDA receptor antibodies in their serum and cerebrospinal fluid (CSF). Results Four of the five cases positive for anti-N-methyl-D-aspartic acid (NMDA) receptor antibodies were di-agnosed with anti-NMDA receptor encephalitis and one was diagnosed with Herpes Simplex Virus Encephalitis(HSE). The five cases had a similar disease presentation including prodromal flu-like symptoms in three cases and psychiatric symptoms at onset in three cases. Four cases developed epilepsy and respiratory failure during the disease course and received treatment in the NICU. Four cases had movement disorders during the late stage of isease..Electroencephalo-graphs and brain MRI showed abnormalities in most cases. The virus infection and dysimmunity test were positive in four cases. Patients with the anti-NMDA receptor encephalitis could have a good immediate prognosis after treatment with hormone and immune globulin. However, two cases developed cancer and one case died during one year fol-low-up. Conclusion Patients with HSE may also test positive for anti-NMDA receptor antibodies. Thus, diagnosis of anti-NMDA receptor encephalitis requires a thorough evaluation including patient’s history and disease course to avoid misdiagnosis.
ABSTRACT
Objectives To investigate the pathogenic mechanism of herpes simplex encephalitis (HSE) and the mecha-nism of action of dexamethasone and acyclovir. Methods 102 male mice were randomly assigned to normal control group, HSV-1 infection group, acyclovir-treated group and combination-treated group. The model of HSE was established by in-tracranial injection of HSV-1 in mice except normal controls. One day after intracranial injection, mice in acyclovir-treated group and combination-treated group were intragastrically administrated with acyclovir, and mice in normal control group and HSV-1 infection group were intragastrically administrated with normal saline. Three days after intracranial injection, mice in combination-treated group were intraperitoneally injected with dexamethasone and mice in other groups were in-traperitoneally injected with normal saline. The neurological injury score and the expressions of IL-2 and IL-10 of the mice brain tissues in each group were compared at 3, 6 and 9 days after model establishment. Results The survival rate of mice was lowest in HSV-1 infection group and highest in combination-treated group (P0.05). Conclusions In comparison with acyclovir monotherapy, combined treatment with dexamethasone and acyclovir for HSE can reduce the expression of IL-2 and IL-10, relieve the clinical symptoms, and increase the survival rate.
ABSTRACT
Relapse of herpes simplex virus (HSV) encephalitis rarely occurs after acyclovir treatment. We experienced a case of relapsing HSV encephalitis in the contralateral temporal lobe, resulting in Kluver-Bucy syndrome, after a full dose acyclovir treatment. Sudden behavioral and emotional changes after HSV encephalitis treatment suggest relapsing HSV encephalitis as well as temporal lobe epilepsy.
Subject(s)
Acyclovir , Encephalitis , Encephalitis, Herpes Simplex , Herpes Simplex , Kluver-Bucy Syndrome , Methylmethacrylates , Polystyrenes , Recurrence , Simplexvirus , Temporal LobeABSTRACT
Objective To analyze clinical characteristics of 8 cases of MELAS syndrome that misdiagnosed as herpes simplex virus encephalitis(HSE).Methods The clinical data of 8 cases of MELAS syndrome that misdiagnosed as HSE were reviewed retrospectively.Results The main manifestations of 8 cases were repeated fever,progressive mental impairment,seizures,headache,descent of eyesight and hearing,weakness of extremities.Fever was the common symptom in the 8 cases.Exercise tolerance dose of serum lactic acid levels studied in 8 cases were obviously abnormal.Imaging examinations showed laminar necrosis or atrophy in brain lobes and basal ganglia areas.Electroencephalogram(EEG) mainly showed diffused slow waves,1 patient displayed myogenic injury in electromyogram(EMG).Muscle biopsy showed red ragged fibers and abnormal mitochondria in all cases.Conclusions The clinical manifestations of MELAS syndrome are similar to HSE,but EEG and imaging results are obviously different from HSE.Exercise tolerance dose of serum lactic acid and muscle biopsy are important for diagnose of MELAS syndrome.