Rm. Harper et al., Lateralized and widespread brain activation during transient blood pressure elevation revealed by magnetic resonance imaging, J COMP NEUR, 417(2), 2000, pp. 195-204
The location and possible lateralization of structures mediating autonomic
processing are not well-described in the human. Functional magnetic resonan
ce imaging procedures were used to demonstrate signal changes in multiple b
rain sites during blood pressure challenges. Magnetic resonance signals in
brain tissue were visualized with a 1.5 Tesla scanner in 11 healthy volunte
ers (22-37 years), by using echo-planar procedures. Images were collected d
uring baseline states and three presser challenges: cold application to the
hand or forehead, and a Valsalva maneuver. Image values from experimental
conditions were compared with corresponding baseline values on a voxel-by-v
oxel basis to identify brain regions responsive to physiologic activation.
Probability maps (P < 0.01) of voxel changes, with Bonferroni corrections f
or multiple comparisons, were determined, and amplitude of signal changes a
ssociated with significance maps were pseudocolored and overlaid on anatomi
c images. The time courses and extent of signal alterations in defined unil
ateral regions were followed and compared with changes in corresponding reg
ions on the contralateral side. Presser challenges elicited significant reg
ional signal intensity changes within the orbitomedial prefrontal cortex, t
emporal cortex, amygdala, hippocampal formation, thalamus, and hypothalamus
. Cerebellar, midbrain, and pontine areas were also recruited. Signal chang
es, especially at forebrain sites, were often highly lateralized. The findi
ngs indicate that (1) transient, behaviorally-coupled cardiovascular challe
nges elicit discrete activity changes over multiple brain sites, and (2) th
ese activity changes, especially in specific prefrontal and temporal forebr
ain regions and cerebellum, are often expressed unilaterally, even to a bil
ateral challenge. J. Comp. Neurol. 417:195-204, 2000. (C) 2000 Wiley-Liss,
Inc.