Ipsilateral versus contralateral cortical motor projections to a shoulder adductor in chronic hemiparetic stroke: implications for the expression of arm synergies.

An increase in ipsilateral descending motor pathway activity has been reported following hemiparetic stroke. In axial muscles, increased ipsilateral cortical activity has been correlated with good recovery whereas in distal arm muscles it is correlated with poor recovery. Currently, little is known about the control of proximal upper limb muscles following stroke. This muscle group is less impaired than the distal arm muscles following stroke, yet contributes to the abnormal motor coordination patterns associated with movements of the arm which can severely impair reaching ability. This study used transcranial magnetic stimulation (TMS) to evaluate the presence and magnitude of ipsilateral and contralateral projections to the pectoralis major (PMJ) muscle in stroke survivors. A laterality index (LI) was used to investigate the relationship between ipsilateral and contralateral projections and strength, clinical impairment level, and the degree of abnormal coordination expressed in the arm. The ipsilateral and contralateral hemispheres were stimulated using 90% TMS intensity while the subject generated shoulder adduction torques in both arms. Motor evoked potentials (MEPs) were measured in the paretic and non-paretic PMJ. The secondary torque at the elbow was measured during maximal adduction as an indicator of the degree of extensor synergy. Ipsilateral MEPs were most common in stroke survivors with moderate to severe motor deficits. The LI was correlated with clinical impairment level (P = 0.05) and the degree of extension synergy expressed in the arm (P = 0.03). The LI was not correlated with strength. These results suggest that increased excitability of ipsilateral pathways projecting to the proximal upper arm may contribute to the expression of the extension synergy following stroke. These findings are discussed in relation to a possible unmasking or upregulation of oligosynaptic cortico-bulbospinal pathways following stroke.