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Cortical Activity in Relation to Velocity Dependent Movement Resistance in the Flexor Muscles of the Hand After Stroke

Department of Rehabilitation Medicine, Danderyd Hospital, Stockholm, Sweden, Pavel.Lindberg{at}rehab.uu.se, Department of Woman and Child Health, Karolinska Institute, Stockholm, Sweden, Department of Neuroscience, Uppsala University Hospital, Uppsala, Sweden

Johan Gäverth, MSc

Department of Rehabilitation Medicine, Danderyd Hospital, Stockholm, Sweden

Anders Fagergren, PhD

Department of Woman and Child Health, Karolinska Institute, Stockholm, Sweden

Peter Fransson, PhD

MR Research Center, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden

Hans Forssberg, PhD

Department of Rehabilitation Medicine, Danderyd Hospital, Stockholm, Sweden

Jörgen Borg, PhD

Department of Neuroscience, Uppsala University Hospital, Uppsala, Sweden

Background. 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.

Key Words: Stroke • Spasticity • Stretch reflex • Functional MRI

This version was published on October 1, 2009

Neurorehabilitation and Neural Repair, Vol. 23, No. 8, 800-810 (2009)
DOI: 10.1177/1545968309332735


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