Hashimoto's encephalitis associated with AMPAR2 antibodies: a case report

被引:8
作者
Zhu, Mingqin [1 ,2 ]
Yu, Xuefan [1 ,2 ]
Liu, Caiyun [1 ,2 ]
Duan, Chenchen [1 ,2 ]
Li, Chunxiao [1 ,2 ]
Zhu, Jie [3 ]
Zhang, Ying [1 ,2 ]
机构
[1] Jilin Univ, Hosp 1, Dept Neurol, Xinmin St 71, Changchun 130000, Peoples R China
[2] Jilin Univ, Hosp 1, Ctr Neurosci, Xinmin St 71, Changchun 130000, Peoples R China
[3] Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Neurodegernerat, SE-14157 Stockholm, Sweden
关键词
Limbic encephalitis; Autoimmune thyroid disease; AMPAR; Hashimoto's thyroiditis; Hashimoto's encephalitis; Case report; RECEPTOR ANTIBODIES; CASE SERIES; ENCEPHALOPATHY; THYROIDITIS; PLASTICITY; DISEASE; CSF;
D O I
10.1186/s12883-017-0823-4
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Hashimoto's encephalitis (HE) is a rare neurological complication of Hashimoto's thyroiditis (HT), while limbic encephalitis (LE) is an autoimmune inflammatory disorder frequently associated with anti-neuronal antibodies. The glutamate receptor a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) is important for synaptic transmission, memory, and learning. The etiology of HE remains unclear. We present a case of HE with antibodies to AMPAR2 both in the serum and cerebrospinal fluid. Case presentation: The patient presented with progressive memory loss and subsequently went into a coma. Magnetic resonance imaging revealed temporal lobe and hippocampal lesions, while the electrocardiogram showed paroxysmal delta waves. Elevated serum levels of antibodies against thyroid globulin, thyroid peroxidase, and thyroid stimulating receptor were also noted. Ultrasonography showed enlargement of the thyroid gland. Therefore, the diagnosis was established as HE. Both the CSF and serum samples of the patient tested positive for antibodies to the cell-surface antigen AMPAR2. Intravenous injection of immunoglobulin followed by dexamethasone treatment resulted in recovery from the coma. Follow-up examination three months later showed some improvement of memory. To our knowledge, this is the first report on the detection of AMPAR2 antibodies in HE. Conclusions: Our findings suggest that antibodies to AMPAR2 may be involved in the pathogenesis of HE. Elevated levels of thyroid antibodies possibly cause immune dysfunction, leading to the production of anti-AMPAR2 antibodies that are detrimental to the neurons. We believe that encephalitis patients with thyroid abnormalities should undergo screening for anti-neuronal antibodies, and early immune therapy may improve prognosis.
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页数:5
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