Purpose: To evaluate the effect of total cerebral infarction volume on motor status and treatment responses to Constraint-Induced Movement therapy (CI therapy) in patients with chronic post-stroke hemiparesis and limb nonuse. In most studies of clinical-radiological correspondences, infarct volume has been found to predict clinical status.
Methods: 60 adult patients who met inclusion criteria for CI therapy underwent standard structural brain MRI around the time of treatment. We tested whether the total volume of infarcted tissue predicted pre-treatment values and pre- to post-treatment changes on standard assessments of laboratory- and real-world-based upper extremity movement.
Results: The patients significantly improved from baseline clinical motor measures after CI therapy. The range of infarction volumes was comparable to those of other stroke studies. In contrast, total infarction volume was not correlated with any of the motor measures. The absence of correlation was maintained even when evaluating only patients with either unilateral or solitary cerebral infarctions, or with respect to severity of baseline motor impairment or variations in the forms of therapy.
Conclusion: The findings suggest that certain standard motor measures in chronic hemiparetic stroke (limb movement in the laboratory, limb use in the life situation, changes in these measures following efficacious CI therapy) are insensitive to infarction load. Our findings are consistent with the hypothesis that plastic brain reorganization after stroke attenuates the effect of infarct volume on purposive limb movement. However, we cannot exclude the possibilities that the specific methods we used to assess upper limb status may be generally insensitive to infarction load, or that the stringent inclusion criteria for this research precluded detecting an effect of infarction load. Further study to evaluate these relationships in the acute-subacute stroke phases and among patients with more severe motor deficits would help to clarify the basis for the lack of an infarction load effect.