Prachi Mehndiratta, MD

Motor recovery after stroke has been correlated with rewiring and connection of ancillary pathways in the brain. This has been demonstrated in a sophisticated and complex manner by utilization of novel MRI techniques. Resting state functional connectivity (rFSC) is one such technique that measures the resting state MRI signals between any pair of brain regions. In patients with subcortical infarcts the bilateral motor cortex rFSC has been shown to undergo a dynamic evolution albeit over a varied time period ranging from 24 hours to a few weeks. The authors of this study chose to study subjects with chronic subcortical stroke > 6 months and excellent motor outcome as by that time structural and functional recovery is nearly stable. They aimed to identify a correlation between the rFSC of bilateral motor cortices (M1-M1) and fractional anisotropy  (FA) of the corticospinal tract (CST) as a measure of motor recovery. 


Sixteen controls and 20 chronic subcortical first-ever ischemic strokes with good motor recover and a Fugl Meyer score > 90/100, were selected for multimodal MRI imaging. FA of CST, M1-M1 anatomical connections and rFSC between M1-M1 cortices were measured.  Diffusion tensor imaging was obtained based on an elaborate but standard protocol and tractography was performed. Motor cortices or Brodman areas 4 were identified a region of interest based rFSC analysis was performed. For each individual dataset, the Pearson correlation coefficient between the mean time series of the left and right ROIs were computed and converted to z value using Fisher’s r-to-z transformation to improve the normality. Then, the general linear model (GLM) was applied to quantitatively compare group differences in the rsFC between stroke patients and healthy controls. In this process, age and sex were treated as covariates of no interest. Differences between two groups were considered significant if P < 0.05. Correlation analysis was performed to assess the relationship between the FA values of the affected CST and the M1-M1 rFSC.

Patients with stroke and healthy controls did not differ demographically. Stroke lesions were in the basal ganglia, thalamus, internal capsule and corona radiata, 9 on the right and 11 in the left hemisphere. Median Fugl Meyer score was  94/100 consistent with excellent motor recovery. Stroke patients with good outcomes demonstrated an increased rFSC M1-M1 connectivity and this was negatively correlated with the FA of the affected CST.

How does one understand these results? In simple terms, a subcortical stroke in the whereabouts of the corticospinal tract results in decreased fractional anisotropy of the tract itself. Increased rFSC represents an attempt by the brain to bypass the affected CST and improve motor cortex connectivity. The rFSC hence is a compensatory mechanism towards motor recovery.  This is a rather complex study, with small number of patients but it re-enforces that neural plasticity is of key importance in stroke recovery. Overall, it is very reassuring to know that the brain is connecting via alternate pathways!