Neuronal integrity is altered in the ipsilesional hand sensory territory in late stroke

BackgroundSensorimotor remapping plays a crucial role in the rehabilitation of hand function after stroke. While motor remapping has been intensively investigated at various levels, from functional to metabolic, limited attention has been given to somatosensory cortical remapping. This study extends our previous work showing functionally relevant metabolic alterations in radiologically normal-appearing or spared motor cortices, predominantly in the ipsilesional (stroke-injured) hemisphere, during the chronic phase of stroke. Precisely, we investigated the metabolic status of the ipsilesional primary somatosensory cortex (S1) and its relation to hand impairment in late stroke. MethodsFourteen individuals with a chronic (mean {+/-} SD, 21.1 {+/-} 36.9 months post-onset) ischemic subcortical stroke, exhibiting moderate hand impairment (Fugl-Meyer Upper Extremity, 44.8 {+/-} 20.9; Jamar dynamometer, 54.1% {+/-} 40.9% of the non-paretic hand), but without sensory deficits, and ten matched healthy controls participated. MR Spectroscopy markers of neuronal status (N-acetylaspartate) and neuronal-glial glutamatergic cycle/neurotransmission (glutamate-glutamine complex) were measured in the ipsilesional S1 (3T, Allegra Siemens Medical Solutions, Erlangen, Germany). Between-group comparison of brain-tissue-corrected levels of these markers (LCModel, SPM12, MATLAB 2023a) and correlation analyses were performed (SPSS v26). ResultsCompared with controls, patients showed significantly lower N-acetylaspartate levels (by 14.5%, p = 0.03) but no significant alterations in glutamate-glutamine levels (by -4.0%, p = 0.6). Significant correlations were found between N-acetylaspartate and the glutamate-glutamine complex in patients (p = 0.02), but not in controls (p = 0.06). No significant correlations were found between S1 markers and hand impairment (p > 0.05 for all). ConclusionsOur findings demonstrate neuronal mitochondrial dysfunction, which correlates with lower cortical excitability in the ipsilesional S1 in chronic stroke survivors. Further work on the functional relevance of such findings, using larger sample sizes, is warranted.