Somatosensory cortex neuronal integrity is altered after stroke

Background Sensorimotor remapping plays a crucial role in hand function rehabilitation 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 in stroke, showing functionally relevant metabolic alterations in radiologically normal-appearing or spared motor cortices, predominantly in the ipsilesional (stroke-injured) hemisphere. We investigated the metabolic status of the ipsilesional primary somatosensory cortex (S1) and its relation to hand impairment after a stroke. Methods Fourteen individuals with a subacute-to-chronic ischemic subcortical stroke leading to a moderate hand/arm motor impairment (Fugl-Meyer Upper Extremity, Jamar dynamometer), but without sensory deficits (Semmes-Weinstein monofilaments), and 10 matched healthy controls participated. MR Spectroscopy markers of neuronal integrity (N-acetylaspartate) and neuronal-glial glutamatergic cycle/neurotransmission (glutamate-glutamine complex) were measured in the ipsilesional radiologically normal-appearing S1 hand territory (3 T, Allegra Siemens Medical Solutions, Erlangen, Germany). Multivariate models (SAS v 9.4) with covariates such as age, sex, and time since stroke were used for the entire patient group. A patient subgroup analysis ( n = 7 in each) was also performed: subacute (≤6 months after onset) and chronic (>6 months). Results Compared with controls, the patient group showed significantly lower N-acetylaspartate levels, with greater alterations in the subacute subgroup. No significant alterations in glutamate-glutamine levels were found in patients. N-acetylaspartate was significantly correlated with glutamate-glutamine in patients, but not in controls. Significant correlations between N-acetylaspartate and hand impairment were found in those with chronic stroke. Conclusion Our preliminary findings suggest neuronal mitochondrial dysfunction, which correlates with reduced cortical excitability in the ipsilesional S1 across subacute and chronic phases of stroke. S1 neuronal dysfunction positively correlates with hand impairment in the chronic but not in the subacute phase of disease. Future longitudinal work with larger sample sizes is warranted.