Evidence map›Paper›PMID 39984138›Full record

ArticleBrain, behavior, and immunity2025

Distinctive seizure signature in the first video case-control study of a naturally-occurring feline autoimmune encephalitis model.

S N M Binks, A H Crawford, E Ives, L J Davison, A Fower, H Fox, A Kaczmarska, M Woodhall, P Waters, A E Handel and 5 more

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Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

S N M BinksOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK; Department of Neurology, John Radcliffe Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford OX3 9DU, UK. Electronic address: sophie.binks@ndcn.ox.ac.uk.
A H CrawfordThe Royal Veterinary College, Hertfordshire AL9 7TA, UK.
E IvesAnderson Moores Veterinary Specialists, Winchester, Hampshire SO21 2LL, UK.
L J DavisonThe Royal Veterinary College, Hertfordshire AL9 7TA, UK; Department of Anatomy, Physiology and Genetics, University of Oxford, Sherrington Building, Sherrington Rd, Oxford OX1 3PT, UK.
A FowerOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
H FoxOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
A KaczmarskaUniversity of Glasgow, School of Biodiversity, One Health and Veterinary Medicine, Small Animal Hospital, 464 Bearsden Rd, Glasgow G61 1QH, UK.
M WoodhallOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
P WatersOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
A E HandelOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
S R IraniOxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK; Departments of Neurology and Neurosciences, Mayo Clinic, Jacksonville, FL, USA.
R Gutierrez QuintanaUniversity of Glasgow, School of Biodiversity, One Health and Veterinary Medicine, Small Animal Hospital, 464 Bearsden Rd, Glasgow G61 1QH, UK.
F A ChowdhuryNeurology, National Hospital for Neurology and Neurosurgery, London, UK; Department of Clinical and Experimental Epilepsy, UCL Institute of Neurology, University College London, London, UK.
S H ErikssonUniversity Clinic for Small Animals, University of Veterinary Medicine, Vienna, Austria.
A PakozdyUniversity Clinic for Small Animals, University of Veterinary Medicine, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveAutoimmune encephalitis (AE) is a form of brain inflammation where pathogenic autoantibodies bind surface proteins. In humans, AE is at least as common as infective encephalitis, and seizures are a prominent manifestation. The most common adult human AE is associated with antibodies to leucine-rich glioma-inactivated 1 (LGI1-Ab-E). AE in non-human mammals is also recognised, notably the polar bear 'Knut', diagnosed with N-methyl D-aspartate receptor antibody encephalitis. LGI1-Ab-E is an emerging cause of spontaneously-arising AE in domestic cats. Our objective was to phenotype the seizure profile of feline LGI1-Ab-E and probe parallels to its human counterpart.

methodsWe characterised seizures in naturally-occurring feline LGI1-Ab-E. Three veterinary and two human neurologists independently blind-rated 35 LGI1-antibody positive and negative feline seizure videos from 24 cats (16 LGI1-Ab-E positive, 8 negative). Data analysed included seizure frequency, semiologies and their co-occurrence, localisation, inter-rater agreement, and predictive factors.

resultsThe mean number of daily seizures at peak was significantly higher in LGI1-antibody positive compared to LGI1-antibody-negative cats (12.6 vs. 1.9/day, pcorr = 0.011). Semiologies statistically significantly enriched in LGI1-Ab-E observations included orofacial automatisms (88/120, 73 % vs. 26/55, 47 %, pcorr = 0.024), salivation (87/120, 73 % vs. 23/55, 42 %, pcorr = 0.004); and mydriasis (79/120, 66 % vs 19/55, 35 %, pcorr = 0.004), and almost exclusively seen in LGI1-Ab-E were circling (39/120, 33 % vs. 1/55, 2 %, pcorr=<0.001) and aggression (14/120, 12 % vs. 0/55, 0 %, non significant after correction). A temporal lobe onset was proposed in 67 % (80/120) of seropositive ratings, compared to 28 % (15/55) LGI1-Ab-E negative (p < 0.0001). Network analysis depicted complex and overlapping relationships between features, akin to the frequent and multifaceted seizures of human LGI1-Ab-E. Orofacial automatisms, mydriasis and temporal lobe localisation were predictive semiological features of feline LGI1-Ab-E. SIGNIFICANCE: Feline LGI1-Ab-E represents a clinically distinctive seizure disorder. Our findings highlight the value of studying naturally-occurring, biologically representative animal models which closely mimic human diseases. This bidirectional translational approach confers benefits across species and unites human and veterinary neurology.

Indexed as

Cat DiseasesEncephalitisHashimoto DiseaseSeizuresAnimalsAutoantibodiesCase-Control StudiesCatsDisease Models, AnimalFemaleIntracellular Signaling Peptides and ProteinsMaleVideo Recordinganti-leucine-rich glioma-inactivated 1 autoantibodyAutoantibodiesIntracellular Signaling Peptides and ProteinsAutoimmuneCatsEncephalitisLeucine-rich glioma-inactivated 1 (LGI1)OrofacialSeizures

Identifiers

PMID39984138
PMCPMC12037459

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.