Structural Changes in the Corticospinal Tract of the Contralesional Hemisphere following Perinatal Lesions

Background/Purpose: In the case of perinatal unilateral brain lesions, damage to the corticospinal tract (CST) can be compensated by the persistence of (usually transient) ipsilateral tract projections. We analyzed diffusion-weighted MRI using fixel-based analysis (FBA) to assess how these lesions affect the ipsi- and contralesional CST, depending on the projection type from the contralesional hemisphere to the paretic hand. In patients with persistent ipsilateral projections (IPSI), we expected an increase of FBA metrics in the contralesional CST as compared with typically developing (TD) controls and patients with “normal” contralateral projections (CONTRA).

Methods: We examined 15 patients (8–26 years, median: 15) with perinatal unilateral brain lesions and 38 controls (8–29 years, median: 16). Anatomical and diffusion-weighted MRI data (p-values = 0/1,000) were acquired using 1.5 T MRI scanners at two study sites. CST wiring pattern was determined with transcranial magnetic stimulation. FBA metrics were obtained by fixel-based whole-brain and tract-specific analyses by means of MRtrix3/-Tissue software. Site, sex, and age at scan were included as nuisance regressors.

Results: Whole-brain analysis revealed a significantly reduced fiber density and cross-section (FDC) metric in the ipsilesional CST across patient groups and an increase in FDC of the contralesional CST only in patients of group IPSI compared with group TD ([Fig. 1A]). Tract-specific analysis further expanded these findings: patients of group IPSI (n = 7) exhibited a significantly increased FDC in the contralesional CST when compared both with group TD and group CONTRA (n = 5) ([Fig. 1B]).

Conclusion: Perinatal unilateral brain lesions lead to detectable white matter changes along the contralesional CST, particularly in patients with an ipsilateral CST wiring pattern. How far these reflect a compensatory potential remains to be elucidated.