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Background <p>Anti-LGI1 encephalitis is a subtype of autoimmune encephalitis characterised by cognitive dysfunction, psychiatric disorders, faciobrachial dystonic seizures, and hyponatraemia. However, its precise pathogenesis remains unclear. Brucellosis, a zoonotic disease prevalent globally, poses a significant threat to public health; nevertheless, the nonspecific nature of its clinical symptoms often results in diagnostic delays.</p> Case presentation <p>We report the case of a middle-aged male patient diagnosed with anti-LGI1 antibody encephalitis through antibodies in serum and CSF combined with neurobrucellosis through serum antibodies and CSF NGS. Additional testing for paraneoplastic-related and demyelinating-related antibodies, CSF and blood culture yielded negative results, helping rule out other pathogens and etiologies. The patient exhibited symptom improvement after effective antimicrobial and immunomodulatory therapies.</p> Conclusions <p>This case raises awareness of autoimmune encephalitis following Brucella infection, revealing a potential association between Brucella infection and anti-LGI1 antibody encephalitis. Brucella may be a triggering factor for anti-LGI1 antibody encephalitis; however, more cases are needed to confirm our findings.</p>

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Dual diagnosis of neurobrucellosis and Anti-LGI1 encephalitis: a rare case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月28日

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  • Chuyan Yang,
  • Ying Liu,
  • Yongzhong Lin,
  • PeiYu Shi,
  • Jing Tan

摘要

Background

Anti-LGI1 encephalitis is a subtype of autoimmune encephalitis characterised by cognitive dysfunction, psychiatric disorders, faciobrachial dystonic seizures, and hyponatraemia. However, its precise pathogenesis remains unclear. Brucellosis, a zoonotic disease prevalent globally, poses a significant threat to public health; nevertheless, the nonspecific nature of its clinical symptoms often results in diagnostic delays.

Case presentation

We report the case of a middle-aged male patient diagnosed with anti-LGI1 antibody encephalitis through antibodies in serum and CSF combined with neurobrucellosis through serum antibodies and CSF NGS. Additional testing for paraneoplastic-related and demyelinating-related antibodies, CSF and blood culture yielded negative results, helping rule out other pathogens and etiologies. The patient exhibited symptom improvement after effective antimicrobial and immunomodulatory therapies.

Conclusions

This case raises awareness of autoimmune encephalitis following Brucella infection, revealing a potential association between Brucella infection and anti-LGI1 antibody encephalitis. Brucella may be a triggering factor for anti-LGI1 antibody encephalitis; however, more cases are needed to confirm our findings.