Brain activation during executed (EM) and imagined movements (IM) of the right and left hand was studied in 10 healthy right-handed subjects using functional magnetic resonance imagining (fMRI). Low electromyographic (EMG) activity of the musculi flexor digitorum superficialis and high vividness of the imagined movements were trained prior to image acquisition. Regional cerebral activation was measured by fMRI during EM and IM and compared to resting conditions. Anatomically selected regions of interest (ROIs) were marked interactively over the entire brain. In each ROI activated pixels above a t value of 2.45 (p < 0.01) were counted and analyzed. In all subjects the supplementary motor area (SMA), the premotor cortex (PMC), and the primary motor cortex (M1) showed significant activation during both EM and IM; the somatosensory cortex (S1) was significantly activated only during EM. Ipsilateral cerebellar activation was decreased during IM compared to EM. In the cerebellum, IM and EM differed in their foci of maximal activation: Highest ipsilateral activation of the cerebellum was observed in the anterior lobe (Larsell lobule H IV) during EM, whereas a lower maximum was found about 2-cm dorsolateral (Larsell lobule H VII) during IM. The prefrontal and parietal regions revealed no significant changes during both conditions. The results of cortical activity support the hypothesis that motor imagery and motor performance possess similar neural substrates. The differential activation in the cerebellum during EM and IM is in accordance with the assumption that the posterior cerebellum is involved in the inhibition of movement execution during imagination.

The causes underlying phantom limb pain are still unknown. Recent studies on the consequences of nervous system damage in animals and humans reported substantial reorganization of primary somatosensory cortex subsequent to amputation, and one study showed that cortical reorganization is positively correlated with phantom limb pain. This paper examined the hypothesis of a functional relationship between cortical reorganization and phantom limb pain. Neuroelectric source imaging was used to determine changes in cortical reorganization in somatosensory cortex after anesthesia of an amputation stump produced by brachial plexus blockade in six phantom limb pain patients and four pain-free amputees. Three of six phantom limb subjects experienced a virtual elimination of current phantom pain attributable to anesthesia (mean change: 3.8 on an 11-point scale;Z= −1.83;p< 0.05) that was mirrored by a very rapid elimination of cortical reorganization in somatosensory cortex (change = 19.8 mm;t₍₂₎= 5.60;p< 0.05). Cortical reorganization remained unchanged (mean change = 1.6 mm) in three phantom limb pain amputees whose pain was not reduced by brachial plexus blockade and in the phantom pain-free amputation controls. These findings suggest that cortical reorganization and phantom limb pain might have a causal relationship. Methods designed to alter cortical reorganization should be examined for their efficacy in the treatment of phantom limb pain.

The main objective of this study is to review and summarize recent findings on electroencephalographic patterns in individuals with chronic pain. We also discuss recent advances in the use of quantitative Electroencephalography (qEEG) for the assessment of pathophysiology and biopsychosocial factors involved in its maintenance over time. Data collection took place from February 2014 to July 2015 in PubMed, SciELO and PEDro databases. Data from cross-sectional studies and longitudinal studies, as well as clinical trials involving chronic pain participants were incorporated into the final analysis. Our primary findings related to chronic pain were an increase of theta and alpha EEG power at rest, and a decrease in the amplitude of evoked potentials after sensory stimulation and cognitive tasks. This review suggests that qEEG could be considered as a simple and objective tool for the study of brain mechanisms involved in chronic pain, as well as for identifying the specific characteristics of chronic pain condition. In addition, results show that qEEG probably is a relevant outcome measure for assessing changes in therapeutic studies.

Objective To investigate the impact of chronic pain on brain dynamics at rest. Methods Functional connectivity was examined in patients with fibromyalgia (FM) (n = 9) and healthy controls (n = 11) by calculating partial correlations between low-frequency blood oxygen level–dependent fluctuations extracted from 15 brain regions. Results Patients with FM had more positive and negative correlations within the pain network than healthy controls. Patients with FM displayed enhanced functional connectivity of the anterior cingulate cortex (ACC) with the insula (INS) and basal ganglia (p values between .01 and .05), the secondary somatosensory area with the caudate (CAU) (p = .012), the primary motor cortex with the supplementary motor area (p = .007), the globus pallidus with the amygdala and superior temporal sulcus (both p values < .05), and the medial prefrontal cortex with the posterior cingulate cortex (PCC) and CAU (both p values < .05). Functional connectivity of the ACC with the amygdala and periaqueductal gray (PAG) matter (p values between .001 and .05), the thalamus with the INS and PAG (both p values < .01), the INS with the putamen (p = .038), the PAG with the CAU (p = .038), the secondary somatosensory area with the motor cortex and PCC (both p values < .05), and the PCC with the superior temporal sulcus (p = .002) was also reduced in FM. In addition, significant negative correlations were observed between depression and PAG connectivity strength with the thalamus (r = −0.64, p = .003) and ACC (r = −0.60, p = .004). Conclusions These findings demonstrate that patients with FM display a substantial imbalance of the connectivity within the pain network during rest, suggesting that chronic pain may also lead to changes in brain activity during internally generated thought processes such as occur at rest. Abbreviations BOLD = blood oxygen level–dependent; FM = fibromyalgia; HC = healthy control; WHYMPI = West Haven-Yale Multidimensional Pain Inventory; fMRI = functional magnetic resonance imaging; ACC = anterior cingulate cortex; PCC = posterior cingulate cortex; AMYG = amygdala; CAU = caudate; PUT = putamen; INS = insula; M1 = primary motor area; SMA = supplementary motor area; SI = primary somatosensory area; SII = secondary somatosensory area; mPFC = medial prefrontal cortex; PAG = periaqueductal gray; STS = superior temporal sulcus; THA = thalamus