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Predicting Value of Pain and Analgesia: Nucleus Accumbens Response to Noxious Stimuli Changes in the Presence of Chronic Pain – Source: Neuron, Apr 15, 2010

  [ 39 votes ]   [ Discuss This Article ]
By Marwan N Baliki, A Vania Apkarian, et al. • • April 26, 2010

[Note: The study essentially demonstrates a distortion in brain activity of chronic back pain patients. When the heat pain applied in the study to normal & chronic back pain patients was stopped, this was interpreted ‘emotionally’ by the normal brains as relief, but by the chronic pain brains as worse back pain (punishment rather than reward). The distinct difference was noted in all subjects, and the authors suggest it “can be used as an objective marker of chronic pain.” To watch a video by the authors, click here. A review on suggests prompt back pain treatment might avoid a  “chronic nonspecific back pain condition that is difficult to reverse": See “Acute Pain May Hijack the Limbic Brain.”.]

We compared brain activations in response to acute noxious thermal [painful heat] stimuli in controls and chronic back pain (CBP) patients.

Pain perception and related cortical activation patterns were similar in the two groups.

However, nucleus accumbens (NAc) activity differentiated the groups at a very high accuracy, exhibiting phasic and tonic responses with distinct properties. Positive phasic NAc activations at stimulus onset and offset tracked stimulus salience and, in normal subjects, predicted reward (pain relief) magnitude at stimulus offset.

In CBP, NAc activity correlated with different cortical circuitry from that of normals and phasic activity at stimulus offset was negative in polarity, suggesting that the acute pain relieves the ongoing back pain.

The relieving effect was confirmed in a separate psychophysical study in CBP.

Therefore, in contrast to somatosensory pathways, which reflect sensory properties of acute noxious stimuli, NAc activity in humans encodes its predicted value and anticipates its analgesic potential on chronic pain.

Source: Neuron, Apr 15, 2010;66(1),149-160. Baliki MN, Geha PY, Fields HL, Apkarian AV. Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Neurology and Ernest Gallo Clinic & Research Center, University of California San Francisco, Emeryville USA. [E-mail:

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