Understanding another person's experience draws on "mirroring systems," brain circuitries shared by the subject's own actions/feelings and by similar states observed in others. Lately, also the experience of pain has been shown to activate partly the same brain areas in the subjects' own and in the observer's brain. Recent studies show remarkable overlap between brain areas activated when a subject undergoes painful sensory stimulation and when he/she observes others suffering from pain. Using functional magnetic resonance imaging, we show that not only the presence of pain but also the intensity of the observed pain is encoded in the observer's brain-as occurs during the observer's own pain experience. When subjects observed pain from the faces of chronic pain patients, activations in bilateral anterior insula (AI), left anterior cingulate cortex, and left inferior parietal lobe in the observer's brain correlated with their estimates of the intensity of observed pain. Furthermore, the strengths of activation in the left AI and left inferior frontal gyrus during observation of intensified pain correlated with subjects' self-rated empathy. These findings imply that the intersubjective representation of pain in the human brain is more detailed than has been previously thought.

The whole human primary somatosensory (SI) cortex is activated by contralateral tactile stimuli, whereas its subarea 2 displays neuronal responses also to ipsilateral stimuli. Here we report on a transient deactivation of area 3b of the ipsilateral SI during long-lasting tactile stimulation.We collected functional magnetic resonance imaging data witha3Tscanner from 10 healthy adult subjects while tactile pulses were delivered at 1, 4, or 10 Hz in 25 s blocks to three right-hand fingers. In the contralateral SI cortex, activation [positive blood oxygenation level-dependent (BOLD) response] outlasted the stimulus blocks by 20 s, with an average duration of 45 s. In contrast, a transient deactivation (negative BOLD response) occurred in the ipsilateral rolandic cortex with an average duration of 18 s. Additional recordings on 10 subjects confirmed that the deactivation was not limited to the right SI but occurred in the SI cortex ipsilateral to the stimulated hand. Moreover, the primary motor cortex (MI) contained voxels that were phasically deactivated in response to both ipsilateral and contralateral touch.These data indicate that unilateral touch of fingers is associated, in addition to the well known activation of the contralateral SI cortex, with deactivation of the ipsilateral SI cortex and of the MI cortex of both hemispheres. The ipsilateral SI deactivation could result from transcallosal inhibition, whereas intracortical SI-MI connections could be responsible for the MI deactivation. The shorter time course of deactivation than activation would agree with stronger decay of inhibitory than EPSP at the applied stimulus repetition rates.

In the absence of external stimuli, human hemodynamic brain activity displays slow intrinsic variations. To find out whether such fluctuations would be altered by persistent pain, we asked 10 patients with unrelenting chronic pain of different etiologies and 10 sex-and agematched control subjects to rest with eyes open during 3-T functional MRI. Independent component analysis was used to identify functionally coupled brain networks. Time courses of an independent component comprising the insular cortices of both hemispheres showed stronger spectral power at 0.12 to 0.25 Hz in patients than in control subjects, with the largest difference at 0.16 Hz. A similar but weaker effect was seen in the anterior cingulate cortex, whereas activity of the precuneus and early visual cortex, used as a control site, did not differ between the groups. In the patient group, seed pointbased correlation analysis revealed altered spatial connectivity between insulae and anterior cingulate cortex. The results imply both temporally and spatially aberrant activity of the affective painprocessing areas in patients suffering from chronic pain. The accentuated 0.12-to 0.25-Hz fluctuations in the patient group might be related to altered activity of the autonomic nervous system. functional MRI | insula | resting state | autonomic nervous system | human A cute pain has an important protective function and is supported by a well-known brain network comprising the insular cortex, anterior cingulate cortex (ACC), primary and secondary somatosensory cortex, and thalamus (1). When pain becomes chronic, its physiological protective function is lost. Chronic pain decreases the quality of life and interferes with the cognitive, affective, and physical functioning. Although one-fifth of the Western population suffers from chronic pain (2), the underlying brain activity is poorly understood.Extensive meta-analyses (1, 3, 4) indicate that the brain areas related to chronic and acute pain differ to some extent, but no single brain-activity pattern is specific to chronic pain. Morphometric analyses suggest gray-matter loss in many chronic pain conditions, indicating that chronic pain may alter brain structure (5), but in a reversible manner (6).Previous studies on the brain basis of chronic pain have concentrated on abnormal activation sites and strengths following external stimulation. Studies of resting-state brain activity by means of functional magnetic resonance imaging (fMRI) have shown that the connectivity within the default-mode network (7) is altered in chronic pain, together with reduced task-related deactivation within this network (8, 9). Recently, the spectra of the default-mode network were shown to contain more power at 0.05 to 0.1 Hz in patients suffering from diabetic neuropathic pain than in healthy control subjects (9).In the present study, we focused on the resting-state fluctuations and functional connectivity of the affective pain-processing areas, the insula and ACC, in chronic pain. Specifically, we recorded spontaneous fMRI sig...

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