ArticleNeuroImage. Clinical2026
Delayed transcallosal conduction to the lesioned sensorimotor cortex in multiple Sclerosis: A combined TMS 7 T-MRI study.
Article in NeuroImage. Clinical, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIn multiple sclerosis (MS), demyelination and degeneration of transcallosal pathways impair interhemispheric communication. While white matter damage is well documented, the impact of cortical lesions on transcallosal conduction remains unclear.
objectiveTo determine whether cortical lesions in the sensorimotor hand area (SM1‑HAND) contribute to impaired transcallosal motor interaction using ultra‑high‑field MRI and transcranial magnetic stimulation (TMS).
methodsTwenty healthy controls (HCs) and 38 MS patients underwent 7 T structural and diffusion‑weighted MRI. Structural scans were used to identify cortical lesions in SM1‑HAND, while diffusion tensor imaging (DTI) quantified microstructural properties in the transcallosal tract connecting left and right SM1‑HAND. Single‑pulse TMS was delivered to each SM1‑HAND during tonic first dorsal interosseous contraction to measure the ipsilateral silent period (iSP). Corticospinal conduction was measured with contralateral motor‑evoked potentials (MEPs), while the iSP was used to compute transcallosal conduction time (TCT).
resultsAmong MS patients, 41 of 76 hemispheres contained an SM1‑HAND lesion. TCT was significantly prolonged in MS relative to HCs (P < 0.001). In patients, cortical lesions delayed transcallosal conduction from the non‑lesion‑bearing to the lesion‑bearing hemisphere (P = 0.026). This direction-specific delay was associated with an intracortical lesion type (P < 0.001), but not with DTI‑derived microstructural measures (P > 0.05).
conclusionsThe presence of cortical lesions in the sensorimotor cortex affects transcallosal inhibition between homologous sensorimotor regions in MS, slowing the build-up of inhibitory influence on the corticospinal output in the lesioned cortex. This delayed inhibitory build‑up appears to be associated with an intracortical lesion type.
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