IntroductionAutoimmune glial fibrillary acidic protein (GFAP) astrocytopathy is a new form of autoimmunity-mediated central nervous system disease. It is especially easy to misdiagnose when clinical symptoms and cerebrospinal fluid (CSF) indicators are similar to those observed in patients with tuberculous meningitis (TBM).MethodsWe retrospectively analyzed five cases of autoimmune GFAP astrocytopathy that were initially misdiagnosed as TBM.ResultsIn the five reported cases, all but one patient had meningoencephalitis in the clinic, and all patients exhibited increased pressure, lymphocytosis, increased protein levels, and decreased glucose levels in their CSF results and did not have typical imaging findings of autoimmune GFAP astrocytopathy. TBM was the initial diagnosis in all five patients. However, we found no direct evidence of tuberculosis infection, and anti-tuberculosis treatment had inconclusive effects. Following a GFAP antibody test, the diagnosis of autoimmune GFAP astrocytopathy was made.ConclusionWhen there is a suspected diagnosis of TBM but TB-related tests are negative, the possibility of autoimmune GFAP astrocytopathy should be considered.
Background
Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a novel autoimmune encephalitis (AE) first identified in 2007. It provides a new direction for clinicians when encountering unexplained symptoms such as seizures, psychotic behavioral abnormalities, speech disorders, and involuntary movements. Most patients have a good prognosis after immunotherapy, but some may experience relapses.
Case presentation
We report a Chinese female patient diagnosed with anti-NMDAR encephalitis. Over the past 30 years, the patient had experienced eight episodes with seizures as the first symptom, which eventually progressed to autoimmune-associated epilepsy. In the last two episodes, both serum and cerebrospinal fluid of the patient were negative for AE-related antibodies, and brain magnetic resonance imaging (MRI) revealed abnormal hyperintensity in the bilateral hippocampi. The patient's symptoms were poorly controlled by immunotherapy but well controlled by anti-seizure medicines.
Conclusions
Patients with a long history of AE and multiple relapses that start with seizures may display alterations of brain structure. Physicians should pay attention to autoimmune-associated epilepsy.
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