Correlation between spasticity and corticospinal/corticoreticular tract status in stroke patients after early stage

Abstract

We investigated the correlation between spasticity and the states of the corticospinal tract (CST) and corticoreticular tract (CRT) in stroke patients after early stage. Thirty-eight stroke patients and 26 healthy control subjects were recruited. The modified Ashworth scale (MAS) scale after the early stage (more than 1 month after onset) was used to determine the spasticity state of the stroke patients. Fractional anisotropy (FA), apparent diffusion coefficient (ADC), fiber number (FN), and ipsilesional/contra-lesional ratios for diffusion tensor tractography (DTT) parameters of the CST and CRT after the early stage were measured in both ipsi- and contra-lesional hemispheres. This study was conducted retrospectively. The FA and FN CST-ratios in the patient group were significantly lower than those of the control group (P < .05), except for the ADC CST-ratio (P > .05). Regarding the DTT parameters of the CRT-ratio, the patient group FN value was significantly lower than that of the control group (P < .05), whereas the FA and ADC CRT-ratios did not show significant differences between the patient and control groups (P > .05). MAS scores showed a strong positive correlation with the ADC CRT-ratio (P < .05) and a moderate negative correlation with the FN CRT-ratio (P < .05). We observed that the injury severities of the CST and CRT were related to spasticity severity in chronic stroke patients; moreover, compared to the CST, CRT status was more closely related to spasticity severity.

Corticospinal tract: a new hope for the treatment of post-stroke spasticity

“…Treatment of PSS has largely focused on reducing the area of cerebral ischemia and rescuing neurons from damaged areas of the brain; however, the effects of putative neuroprotectants are less pronounced in clinical trials [ 5 ]. Several recent clinical studies report that the degree of corticospinal tract (CST) damage correlates with the severity of spasticity in patients with chronic stroke [ 6 – 8 ] and that there is a significant correlation between motor function improvement and CST remodeling in patients with PSS [ 9 ]. A few experimental studies have also observed that by destroying the corresponding CST, the upper motor neurons lose control of the spinal cord, causing spasticity of the contralateral limb [ 10 ].…”