Differences in cortical response to acupressure and electroacupuncture stimuli.

I don't pretend to understand all the ins and outs of brain imaging. From what I can understand, though, is that there is a system of "recruitment" in patients with chronic pain, whereby there is an ever larger area of the brain devoted to the pain stimulus so that it is outsized compared to the actual insult. Acupuncture tends to mitigate this "maladaptive neuroplasticity." I won't comment on the differences between acupressure and acupuncture since I don't feel competent to interpret. (Info on my practice here.)

BMC Neurosci. 2011 Jul 27;12:73.
Differences in cortical response to acupressure and electroacupuncture stimuli.
Witzel T, Napadow V, Kettner NW, Vangel MG, Hämäläinen MS, Dhond RP.
Harvard Medical School, Martinos Center for Biomedical Imaging, Charlestown, MA 02129, USA.
Abstract
BACKGROUND:
FMRI studies focus on sub-cortical effects of acupuncture stimuli. The purpose of this study was to assess changes in primary somatosensory (S1) activity over the course of different types of acupuncture stimulation. We used whole head magnetoencephalography (MEG) to map S1 brain response during 15 minutes of electroacupuncture (EA) and acupressure (AP). We further assessed how brain response changed during the course of stimulation.
RESULTS:
Evoked brain response to EA differed from AP in its temporal dynamics by showing clear contralateral M20/M30 peaks while the latter demonstrated temporal dispersion. Both EA and AP demonstrated significantly decreased response amplitudes following five minutes of stimulation. However, the latency of these decreases were earlier in EA (~30 ms post-stimulus)
than AP (> 100 ms). Time-frequency responses demonstrated early onset, event related synchronization (ERS), within the gamma band at ~70-130 ms and the theta band at ~50-200 ms post-stimulus. A prolonged event related desynchronization (ERD) of alpha and beta power occurred at ~100-300 ms post-stimulus. There was decreased beta ERD at ~100-300 ms over the course of EA, but not AP.
CONCLUSION:
Both EA and AP demonstrated conditioning of SI response. In conjunction with their subcortical effects on endogenous pain regulation, these therapies show potential for affecting S1 processing and possibly altering maladaptive neuroplasticity. Thus, further investigation in neuropathic populations is needed.
Whole article is available here.