The monkey premotor cortex contains neurons that discharge during action execution and during observation of actions made by others. Transcranial magnetic stimulation experiments suggest that a similar observation͞ execution matching system also is present in humans. We recorded neuromagnetic oscillatory activity of the human precentral cortex from 10 healthy volunteers while (i) they had no task to perform, (ii) they were manipulating a small object, and (iii) they were observing another individual performing the same task. The left and right median nerves were stimulated alternately (interstimulus interval, 1.5 s) at intensities exceeding motor threshold, and the poststimulus rebound of the rolandic 15-to 25-Hz activity was quantified. In agreement with previous studies, the rebound was strongly suppressed bilaterally during object manipulation. Most interestingly, the rebound also was significantly diminished during action observation (31-46% of the suppression during object manipulation). Control experiments, in which subjects were instructed to observe stationary or moving stimuli, confirmed the specificity of the suppression effect. Because the recorded 15-to 25-Hz activity is known to originate mainly in the precentral motor cortex, we concluded that the human primary motor cortex is activated during observation as well as execution of motor tasks. These findings have implications for a better understanding of the machinery underlying action recognition in humans.

Our SEDAN score reliably assessed risk for sICH in IV thrombolysis-treated patients with anterior- and posterior circulation ischemic stroke, and it can support clinical decision making in high-risk patients. External validation of the score supports its generalization.

Magnetoencephalography (MEG) is a totally non-invasive research method which provides information about cortical dynamics on a millisecond time-scale. Whole-scalp magnetic field patterns following stimulation of different peripheral nerves indicate activation of an extensive cortical network. At the SI cortex, the responses reflect mainly the activity of area 3b, with clearly somatotopical representations of different body parts. The SII cortex is activated bilaterally and it also receives, besides tactile input, nociceptive afference. Somatically evoked MEG signals may also be detected from the posterior parietal cortex, central mesial cortex and the frontal lobe. The serial versus parallel processing in the cortical somatosensory network is still under debate.

Alterations in tactile sensitivity are common in patients with chronic pain. Recent brain imaging studies have indicated that brain areas activated by acute experimental pain partly overlap with areas processing innocuous tactile stimuli. However, the possible effect of chronic pain on central tactile processing has remained unclear. We have examined, both clinically and with whole-head magnetoencephalography, six patients suffering from complex regional pain syndrome (CRPS) of the upper limb. The cortical somatosensory responses were elicited by tactile stimuli applied to the fingertips and the reactivity of spontaneous brain oscillations was monitored as well. Tactile stimulation of the index finger elicited an initial activation at 65 ms in the contralateral SI cortex, followed by activation of the ipsi- and contralateral SII cortices at about 130 ms. The SI responses were 25-55% stronger to stimulation of the painful than the healthy side. The distance between SI representations of thumb and little finger was significantly shorter in the hemisphere contralateral than ipsilateral to the painful upper limb. In addition, reactivity of the 20-Hz motor cortex rhythm to tactile stimuli was altered in the CRPS patients, suggesting modified inhibition of the motor cortex. These results imply that chronic pain may alter central tactile and motor processing.

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...

We recorded somatosensory evoked magnetic fields from ten healthy, right-handed subjects with a 122-channel whole-scalp SQUID magnetometer. The stimuli, exceeding the motor threshold, were delivered alternately to the left and right median nerves at the wrists, with interstimulus intervals of 1, 3, and 5 s. The first responses, peaking around 20 and 35 ms, were explained by activation of the contralateral primary somatosensory cortex (SI) hand area. All subjects showed additional deflections which peaked after 85 ms; the source locations agreed with the sites of the secondary somatosensory cortices (SII) in both hemispheres. The SII responses were typically stronger in the left than the right hemisphere. All subjects had an additional source, not previously reported in human evoked response data, in the contralateral parietal cortex. This source was posterior and medial to the SI hand area, and evidently in the wall of the postcentral sulcus. It was most active at 70-110 ms.

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