Article

The role of spinal networks in spasticity is well investigated, but
little is known about possible cortical contributions to hypertonicity across a
joint. OBJECTIVE: The authors hypothesized that there are cortical activation
correlates to spasticity in stroke patients with increased muscle tone of the
wrist flexors. METHODS: Stroke patients and controls were scanned using
event-related functional magnetic resonance imaging (fMRI) during slow and fast
passive movements of the hand with simultaneous recording of passive movement
resistance (PMR). RESULTS: Control participants had velocity-dependent activity
(greater for slow than fast movements) of 2 types, in areas that were also more
active in passive movement than rest (eg, relative increase in activation in
contralateral S1 and M1 was greater for slow than fast) and in areas that were
also more active in rest than passive movement (eg, relative decrease in
activation in occipital areas and ipsilateral precentral gyrus was greater for
fast than slow). In the patient group, with large interindividual variation of
spasticity, we found an association between PMR and the velocity-dependent
activity in ipsilateral S1 (area 3b) extending into M1 (area 4a), contralateral
cingulate cortex, supplementary motor area (SMA), Brodmann Area 45 (BA 45), and
cerebellum. Post hoc testing also revealed a similar correlation in S1 and M1
bilaterally in controls and showed that patients activated ipsilateral S1 and M1
more than controls in the velocity-dependent condition. CONCLUSIONS: The findings
suggest the possibility of ipsilateral sensory and motor cortical involvement in
spasticity after stroke, which warrant further investigation.

Langue : ANGLAIS