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Peer-reviewedCC BY 4.0Cureus

Recurrent Aphasic Seizures as the Initial Manifestation of LGI1 Antibody-Associated Autoimmune Limbic Encephalitis Mimicking a Transient Ischaemic Attack: A Case Report

  • Aima Hameed1
  • Jyotsna Kakarla2
  • Siddhi A Gaunekar1
  • Akshayaa K Aggarawal3
  • Ajmal Raoof4
4 affiliations
  1. 1General Internal Medicine, Kettering General Hospital NHS Foundation Trust, Kettering, GBR
  2. 2General Surgery, Queen's Hospital Burton, University Hospitals of Derby and Burton NHS Foundation Trust, Burton-on-Trent, GBR
  3. 3Internal Medicine, Walsall Manor Hospital, Walsall, GBR
  4. 4Internal Medicine, Kettering General Hospital NHS Foundation Trust, Kettering, GBR
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Abstract

We report the case of a 55-year-old man who presented with recurrent, brief episodes of isolated speech arrest lasting 10-30 seconds, during which awareness and comprehension were preserved. Initial neurological examination and neuroimaging were unremarkable, and the episodes were initially attributed to suspected transient ischaemic attacks (TIAs).

Subsequently, the patient developed a generalised tonic-clonic seizure, prompting initiation of antiepileptic therapy. Over the following months, he experienced an increasing frequency of transient aphasic episodes alongside focal seizures with left-sided motor involvement, which proved refractory to multiple antiepileptic medications.

Further investigation during hospital admission revealed significant hyponatraemia and characteristic magnetic resonance imaging (MRI) findings, including bilateral medial temporal lobe enlargement with fluid-attenuated inversion recovery (FLAIR) hyperintensity involving the amygdala and hippocampi. The detection of LGI1 antibodies, in conjunction with the clinical presentation and radiological features, confirmed the diagnosis of LGI1 antibody-associated autoimmune limbic encephalitis.

The patient was treated with intravenous methylprednisolone followed by oral corticosteroid therapy, resulting in a marked reduction in seizure frequency and severity. This case underscores the importance of recognising aphasic seizures as a potential manifestation of autoimmune encephalitis (AIE), particularly LGI1-associated disease, to avoid diagnostic delay and facilitate early initiation of immunotherapy.

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Cite

BibTeXRIS
BibTeX
@article{hameed2026recurrent,
  title = {{Recurrent Aphasic Seizures as the Initial Manifestation of LGI1 Antibody-Associated Autoimmune Limbic Encephalitis Mimicking a Transient Ischaemic Attack: A Case Report}},
  author = {Aima Hameed and Jyotsna Kakarla and Siddhi A Gaunekar and Akshayaa K Aggarawal and Ajmal Raoof},
  journal = {Cureus},
  year = {2026},
  month = sep,
  doi = {10.7759/cureus.116958},
  url = {https://doi.org/10.7759/cureus.116958},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Recurrent Aphasic Seizures as the Initial Manifestation of LGI1 Antibody-Associated Autoimmune Limbic Encephalitis Mimicking a Transient Ischaemic Attack: A Case Report
AU  - Aima Hameed
AU  - Jyotsna Kakarla
AU  - Siddhi A Gaunekar
AU  - Akshayaa K Aggarawal
AU  - Ajmal Raoof
PY  - 2026
DA  - 2026/09/26
JO  - Cureus
DO  - 10.7759/cureus.116958
UR  - https://doi.org/10.7759/cureus.116958
AB  - We report the case of a 55-year-old man who presented with recurrent, brief episodes of isolated speech arrest lasting 10-30 seconds, during which awareness and comprehension were preserved. Initial neurological examination and neuroimaging were unremarkable, and the episodes were initially attributed to suspected transient ischaemic attacks (TIAs).  Subsequently, the patient developed a generalised tonic-clonic seizure, prompting initiation of antiepileptic therapy. Over the following months, he experienced an increasing frequency of transient aphasic episodes alongside focal seizures with left-sided motor involvement, which proved refractory to multiple antiepileptic medications.  Further investigation during hospital admission revealed significant hyponatraemia and characteristic magnetic resonance imaging (MRI) findings, including bilateral medial temporal lobe enlargement with fluid-attenuated inversion recovery (FLAIR) hyperintensity involving the amygdala and hippocampi. The detection of LGI1 antibodies, in conjunction with the clinical presentation and radiological features, confirmed the diagnosis of LGI1 antibody-associated autoimmune limbic encephalitis.  The patient was treated with intravenous methylprednisolone followed by oral corticosteroid therapy, resulting in a marked reduction in seizure frequency and severity. This case underscores the importance of recognising aphasic seizures as a potential manifestation of autoimmune encephalitis (AIE), particularly LGI1-associated disease, to avoid diagnostic delay and facilitate early initiation of immunotherapy.
SN  - 2168-8184
ER  -