BoNT appears to act not in the periphery but also indirectly at supraspinal levels, including modulation of cortical sensorimotor control in disorders such as dystonia and spasticity.

To detect changes in brain activation in patients with post-stroke arm spasticity treated by botulinum toxin A (BoNT) and rehabilitation and studied with functional MRI (fMRI).

31 patients (16 men, 15 women, mean age 58.4) with severe weakness and PSS were studied. Spasticity was assessed using modified Ashworth scale (MAS). FMRI was performed thrice: before BoNT application (W0), 4 weeks (W4) and 11 weeks (W11) after BoNT. FMRI data were acquired during imagery of sequential finger movement with the impaired hand. Group-level modeling included (1) mean activation at individual sessions using MAS and age at W0 as covariates; and (2), BoNT and time since W0 as independent variables. Resulting statistical maps were cluster-thresholded at p = 0.05 corrected.

BoNT treatment was effective in reducing arm spasticity. Mean MAS score were: at W0, 2.40 (SD 0.49), at W4, 1.49 (SD 0.51) and at W11, 2.15 (SD 0.52). FMRI during movement imagery before treatment (W0) demonstrated extensive activation of bilateral frontoparietal sensorimotor cortex, cerebellum and contralesional basal ganglia and thalamus, where peak activation localized to the supplementary motor area, cortex lining the intraparietal sulcus bilaterally (IPS), contralesional ventrolateral premotor cortex and Ipsilesional cerebellar hemisphere. After treatment (W4), the activation pattern showed clear reduction, mostly in the bilateral parietal cortex and cerebellum. After disappearance of the local BoNT effect (W11), activation extent returned to almost the original size. Specific contrast revealed a localized significant BoNT-A effect, manifested as a transient activation decrease in the ipsilesional IPS and superior parietal lobule.

In the course of BoNT therapy of post-stroke arm spasticity, we observed transient changes in hand motor imagery-related brain activation, predominantly in the ipsilesional parietal cortex.