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Updated: May 23, 2026
Magnetic Resonance Imaging of Multiple Sclerosis at 7.0 Tesla
Published on: February 19, 2021
Delayed transcallosal conduction to the lesioned sensorimotor cortex in multiple Sclerosis: A combined TMS 7 T-MRI
Mads A J Madsen1, Lasse Christiansen2, Vanessa Wiggermann3
1Danish Research Centre for Magnetic Resonance, Department of Radiology and Nuclear Medicine, Copenhagen University Hospital -Amager & Hvidovre 2650 Hvidovre, Denmark; MS Center Amsterdam, Anatomy and Neurosciences, Amsterdam UMC location Vrije Universiteit Amsterdam, Amsterdam, the Netherlands; Amsterdam Neuroscience, Neuroinflammation and - Neurodegeneration, Brain Imaging, Amsterdam, the Netherlands.
Cortical lesions in multiple sclerosis (MS) significantly impair interhemispheric communication by delaying transcallosal conduction. This finding highlights the impact of sensorimotor cortex lesions on brain connectivity in MS patients.
Area of Science:
- Neuroscience
- Neuroimaging
- Neurology
Background:
- Multiple sclerosis (MS) involves demyelination and degeneration of white matter, affecting interhemispheric communication.
- The specific impact of cortical lesions on transcallosal conduction in MS remains largely unclear.
Purpose of the Study:
- To investigate if cortical lesions in the sensorimotor hand area (SM1-HAND) contribute to impaired transcallosal motor interaction.
- Utilize ultra-high-field MRI and transcranial magnetic stimulation (TMS) to assess this relationship.
Main Methods:
- 38 MS patients and 20 healthy controls (HCs) underwent 7T MRI and diffusion tensor imaging (DTI).
- Cortical lesions in SM1-HAND were identified, and transcallosal tract microstructural properties were quantified.
- Single-pulse TMS measured ipsilateral silent period (iSP) to calculate transcallosal conduction time (TCT).
Main Results:
- Cortical lesions were present in 41 of 76 MS patient hemispheres.
- Transcallosal conduction time (TCT) was significantly prolonged in MS patients compared to HCs.
- Cortical lesions specifically delayed transcallosal conduction from the non-lesioned to the lesioned hemisphere, linked to intracortical lesion type.
Conclusions:
- Cortical lesions in the sensorimotor cortex disrupt transcallosal inhibition between homologous sensorimotor regions in MS.
- This leads to a slowed build-up of inhibitory influence on corticospinal output in the affected cortex.
- The observed delay is associated with an intracortical lesion type.
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