MR imaging of cerebral activation performed with a gradient-echo technique at 1.5 T: sources of activation signals

MR imaging of cerebral activation has been successfully performed at 1.5 T for functional maps of the brain. However, major sources of activation signals in such imaging remain controversial. The purpose of this study is to investigate anatomic and physiologic sources of activation signals in MR imaging of cerebral activation performed with a gradient-echo technique at 1.5 T.

Motor cortex activation studies (n = 8) were conducted using a gradient-echo technique (80/60 [TR/TE], 40 degrees flip angle). MR venograms were then obtained at the same imaging plane to visualize the cortical veins, which were then compared with the shape and location of the activation signals. To investigate the physiologic sources of activation signal, the activation studies were repeated with different TEs (15, 30, and 60 msec), which allowed us to evaluate the blood oxygen level-dependent effect; with different flip angles (40 degrees and 10 degrees); and without and with presaturation of adjacent sections, all of which allowed us to evaluate inflow effect.

All activation signals were detected in the sulcus just posterior (n = 7) or lateral (n = 1) to the motor cortex. In seven of eight studies, shape and location of these signals corresponded well with those of the cortical veins. In the eighth study, the correspondence was partial. Activation signals significantly increased at a TE of 60 msec (p < .01), suggesting enhancement of the blood oxygen level-dependent effect at a long TE. Activation signals significantly decreased with a 10 degrees flip angle (p < .01) and with presaturation of adjacent sections (p < .01), indicating that the inflow effect was suppressed by a small flip angle and the elimination of unsaturated inflowing protons.

Our results suggest that signals in cerebral activation obtained by MR imaging with a gradient-echo technique at 1.5 T arise mainly from the cortical veins draining the activated cortex. Physiologically, both blood oxygen level-dependent and inflow effects contribute to signal generation.