# T1w/T2w Ratio Identifies the Basolateral Amygdala as a Preferential Target in Autoimmune Limbic Encephalitis

**Authors:** Rakshit Dadarwal, Andre Dik, Laura Bierhansl, Noëmi Gmahl, Nils C. Landmeyer, Tobias J. Brix, Veronika K. Jaeger, Jochen Bauer, Wilhelm Küker, Heinz Wiendl, Christian E. Elger, Stjepana Kovac, Antje Bischof

PMC · DOI: 10.1111/jon.70120 · Journal of Neuroimaging · 2026-01-22

## TL;DR

This study shows that the T1w/T2w MRI ratio can identify specific amygdala damage in autoimmune limbic encephalitis, linked to seizure focus and potential for early diagnosis.

## Contribution

The study introduces the T1w/T2w ratio as a novel noninvasive biomarker for detecting amygdala pathology in ALE.

## Key findings

- The T1w/T2w ratio in the left amygdala was reduced in patients with left or bitemporal epileptic foci.
- The left basolateral amygdala complex showed the most significant T1w/T2w ratio reduction in ALE patients.
- Amygdalar volumes were similar between ALE patients and controls, but the left lateral nucleus volume increased in left temporal ALE.

## Abstract

The amygdala plays a key role in the pathophysiology of autoimmune limbic encephalitis (ALE), contributing to epileptic seizures and neuropsychiatric symptoms. While no study has examined microstructural changes in individual amygdala nuclei in ALE, we used the T1‐weighted/T2‐weighted (T1w/T2w) ratio to explore amygdalar pathology and its associations with clinical manifestations, including epilepsy and neuropsychiatric symptoms.

This single‐center study examined 57 patients diagnosed with ALE and 16 healthy controls (HC). Patients underwent a comprehensive assessment that included clinical, electroencephalogram (EEG), magnetic resonance imaging (MRI), and neuropsychological assessments. Patients were stratified by epileptic focus based on long‐term EEG. T1w/T2w ratio and volumetric measures of the amygdala and its nuclei were analyzed and correlated with epileptic focus and neuropsychiatric outcomes.

EEG revealed 26 left temporal, 26 bitemporal, and five right temporal epileptic foci. The T1w/T2w ratio in the left amygdala was markedly reduced in patients with left temporal (p = 0.013) and bitemporal (p = 0.018) epileptic foci compared to HC. This reduction was most pronounced in the left basolateral complex (p = 0.011). Whereas amygdalar volumes were similar between patients and HC, exploratory analyses showed an increased volume of the left lateral nucleus in left temporal ALE (p = 0.036). Furthermore, we found no correlations between MRI measures and neuropsychiatric scores.

Our findings indicate that the basolateral complex of the amygdala is preferentially affected in ALE, suggesting a region‐specific vulnerability to autoimmune‐mediated inflammation. T1w/T2w ratio alterations reflect the epileptogenic focus and may serve as a clinically accessible, noninvasive biomarker for early diagnosis and treatment monitoring in ALE.

## Linked entities

- **Diseases:** autoimmune limbic encephalitis (MONDO:0850097), epilepsy (MONDO:0005027)

## Full-text entities

- **Genes:** MOG (myelin oligodendrocyte glycoprotein) [NCBI Gene 4340] {aka BTN6, BTNL11, MOGIG2, NRCLP7}, LGI1 (leucine rich glioma inactivated 1) [NCBI Gene 9211] {aka ADLTE, ADPAEF, ADPEAF, DEE121, EPITEMPIN, EPT}
- **Diseases:** neuropsychiatric deficits (MESH:D001289), neurological diseases (MESH:D020271), Epilepsy (MESH:D004827), atrophy (MESH:D001284), mesial temporal lobe epilepsy (MESH:C566903), ASM (MESH:D012640), idiopathic generalized epilepsy (MESH:C562694), neuropsychiatric disorders (MESH:D001523), neurodegeneration (MESH:D019636), -NMDA receptor encephalitis (MESH:D060426), optic neuritis (MESH:D009902), language impairment (MESH:D007806), neuroinflammation (MESH:D000090862), ALE (MESH:C531729), autoimmune encephalitis (MESH:D020274), Neuropsychiatric (MESH:C000631768), autoimmune-mediated inflammatory disease (MESH:D001327), Limbic Encephalitis (MESH:D020363), HC (MESH:D000067329), autoimmune-mediated inflammation (MESH:D007249), mood disorders (MESH:D019964), Anxiety (MESH:D001007), gliosis (MESH:D005911), multiple sclerosis (MESH:D009103), TLE-HS (MESH:D004833), focal epilepsy (MESH:D004828), sudden unexpected death (MESH:D000080485), amygdalar abnormalities (MESH:D000014), anxiety disorders (MESH:D001008), swelling (MESH:D004487), cognitive deficits (MESH:D003072), Depression (MESH:D003866), epilepsy syndrome (MESH:D000073376), hippocampal sclerosis (MESH:D000092223), memory deficits (MESH:D008569), psychosis (MESH:D011618)
- **Chemicals:** iron (MESH:D007501), ASM (-), methylprednisolone (MESH:D008775), N-methyl-D-aspartate (MESH:D016202), mycophenolate mofetil (MESH:D009173), azathioprine (MESH:D001379), steroid (MESH:D013256), rituximab (MESH:D000069283)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12825940/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12825940/full.md

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Source: https://tomesphere.com/paper/PMC12825940