This Article Full Text All Versions of this Article: 34/5/e26    most recent 01.STR.0000071140.00153.05v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Dobkin, B. H. Search for Related Content PubMed PubMed Citation Articles by Dobkin, B. H. Related Collections Computerized tomography and Magnetic Resonance Imaging Rehabilitation, Stroke

(Stroke. 2003;34:e26.)
© 2003 American Heart Association, Inc.

Research Reports

Editorial Comment—Functional MRI: A Potential Physiologic Indicator for Stroke Rehabilitation Interventions

Department of Neurology, David Geffen School of Medicine of the University of California Los Angeles, Neurologic Rehabilitation and Research Program, Reed Neurologic Research Center, Los Angeles, California

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
A patient recovering from a modest hemiparesis from stroke alternates between rest and tapping the affected index finger¹ or gripping a transducer with visual feedback about the force exerted² during functional MRI (fMRI). Do the evoked patterns of cerebral activity reveal the reorganization and rehabilitation of the motor mind? They may, if considered within the context of potentially confounding technical, statistical, anatomical, experiential, and task-dependent factors.^3,4

What Are the General Determinants of fMRI Patterns of Activation Induced By a Movement?
Maps of functional anatomy obtained using the blood-oxygen–level-dependent (BOLD) technique depend on the spatial extent of metabolic and hemodynamic changes induced by local synaptic activity and local field potentials, but do not precisely correlate with such activity.⁵ Localization and spatial resolution of neuronal activity may be confounded by a range of signal-dependent factors. These include BOLD-dependent capillary density and draining veins, perfusion of hemodynamically compromised tissue, links between one active population of neurons to others,⁶ possible differences in the BOLD signal caused by presynaptic inhibition compared with excitation, and fine differences between subjects in the location of regions of interest.⁷ fMRI methods are not a done deal. Some controversy and room for error accompany every aspect of data acquisition and analysis. Choices are made about the MR sequences for scans, data smoothing and correction schemes, registration of activations onto anatomical space especially when an infarct distorts morphology, modeling choices for the statistics represented by colored voxels of activity, statistical inferences, and approaches to individual subject versus group analyses. In addition, physiological factors such as sleep deprivation and estrogen levels and drugs such as caffeine . . . [Full Text of this Article]