Increased EEG power and slowed dominant frequency in patients with neurogenic pain

To study the mechanisms of chronic neurogenic pain, we compared the power spectra of the resting EEG of patients (n = 15, 38-75 years, median 64 years, 6 women) and healthy controls (n = 15, 41-71 years, median 60 years, 8 women). On an average, the patient group exhibited higher spectral power over the frequency range of 2-25 Hz, and the dominant peak was shifted towards lower frequencies. Maximal differences appeared in the 7-9 Hz band in all electrodes. Frontal electrodes contributed most to this difference in the 13-15 Hz band. Bicoherence analysis suggests an enhanced coupling between theta (4-9 Hz) and beta (12-25 Hz) frequencies in patients. The subgroup of six patients free from centrally acting medication showed higher spectral power in the 2-18 Hz frequency range. On an individual basis, the combination of peak height and peak frequency discriminated between patient and control groups: discriminant analysis classified 87% of all subjects correctly. After a therapeutic lesion in the thalamus (central lateral thalamotomy, CLT) we carried out follow-up for a subgroup of seven patients. Median pain relief was 70 and 95% after 3 and 12 months, respectively. The average EEG power of all seven patients gradually decreased in the theta band and approached normal values only after 12 months. The excess theta EEG power in patients and its decrease after thalamic surgery suggests that both EEG and neurogenic pain are determined by tightly coupled thalamocortical loops. The small therapeutic CLT lesion is thought to initiate a progressive normalization in the affected thalamocortical system, which is reflected in both decrease of EEG power and pain relief

Increased EEG power and slowed dominant frequency in patients with neurogenic pain

To study the mechanisms of chronic neurogenic pain, we compared the power spectra of the resting EEG of patients (n = 15, 38-75 years, median 64 years, 6 women) and healthy controls (n = 15, 41-71 years, median 60 years, 8 women). On an average, the patient group exhibited higher spectral power over the frequency range of 2-25 Hz, and the dominant peak was shifted towards lower frequencies. Maximal differences appeared in the 7-9 Hz band in all electrodes. Frontal electrodes contributed most to this difference in the 13-15 Hz band. Bicoherence analysis suggests an enhanced coupling between theta (4-9 Hz) and beta (12-25 Hz) frequencies in patients. The subgroup of six patients free from centrally acting medication showed higher spectral power in the 2-18 Hz frequency range. On an individual basis, the combination of peak height and peak frequency discriminated between patient and control groups: discriminant analysis classified 87% of all subjects correctly. After a therapeutic lesion in the thalamus (central lateral thalamotomy, CLT) we carried out follow-up for a subgroup of seven patients. Median pain relief was 70 and 95% after 3 and 12 months, respectively. The average EEG power of all seven patients gradually decreased in the theta band and approached normal values only after 12 months. The excess theta EEG power in patients and its decrease after thalamic surgery suggests that both EEG and neurogenic pain are determined by tightly coupled thalamocortical loops. The small therapeutic CLT lesion is thought to initiate a progressive normalization in the affected thalamocortical system, which is reflected in both decrease of EEG power and pain relie

Pain Ratings, Psychological Functioning and Quantitative EEG in a Controlled Study of Chronic Back Pain Patients

<div><h3>Objectives</h3><p>Several recent studies report the presence of a specific EEG pattern named Thalamocortical Dysrhythmia (TCD) in patients with severe chronic neurogenic pain. This is of major interest since so far no neuroscientific indicator of chronic pain could be identified. We investigated whether a TCD-like pattern could be found in patients with moderate chronic back pain, and we compared patients with neuropathic and non-neuropathic pain components. We furthermore assessed the presence of psychopathology and the degree of psychological functioning and examined whether the strength of the TCD-related EEG markers is correlated with psychological symptoms and pain ratings.</p> <h3>Design</h3><p>Controlled clinical trial with age and sex matched healthy controls.</p> <h3>Methods</h3><p>Spontaneous EEG was recorded in 37 back pain patients and 37 healthy controls.</p> <h3>Results</h3><p>We were not able to observe a statistically significant TCD effect in the EEG data of the whole patient group, but a subsample of patients with evidence for root damage showed a trend in this direction. Pain patients showed markedly increased psychopathology. In addition, patients' ratings of pain intensity within the last 1 to 12 months showed strong correlations with EEG power, while psychopathology was correlated to the peak frequency.</p> <h3>Conclusion</h3><p>Out of several possible interpretations the most likely conclusion is that only patients with severe pain as well as root lesions with consecutive thalamic deafferentation develop the typical TCD pattern. Our primary method of defining ‘neuropathic pain’ could not reliably determine if such a deafferentation was present. Nevertheless the analysis of a specific subsample as well as correlations between pain ratings, psychopathology and EEG power and peak frequency give some support to the TCD concept.</p> <h3>Trial Registration</h3><p>ClinicalTrials.gov <a href="http://clinicaltrials.gov/ct2/show/NCT00744575">NCT00744575</a></p> </div

Brain rhythms of pain

Pain is an integrative phenomenon that results from dynamic interactions between sensory and contextual (i.e., cognitive, emotional, and motivational) processes. In the brain the experience of pain is associated with neuronal oscillations and synchrony at different frequencies. However, an overarching framework for the significance of oscillations for pain remains lacking. Recent concepts relate oscillations at different frequencies to the routing of information flow in the brain and the signaling of predictions and prediction errors. The application of these concepts to pain promises insights into how flexible routing of information flow coordinates diverse processes that merge into the experience of pain. Such insights might have implications for the understanding and treatment of chronic pain

Temporo-insular enhancement of EEG low and high frequencies in patients with chronic tinnitus. QEEG study of chronic tinnitus patients

<p>Abstract</p> <p>Background</p> <p>The physiopathological mechanism underlying the tinnitus phenomenon is still the subject of an ongoing debate. Since oscillatory EEG activity is increasingly recognized as a fundamental hallmark of cortical integrative functions, this study investigates deviations from the norm of different resting EEG parameters in patients suffering from chronic tinnitus.</p> <p>Results</p> <p>Spectral parameters of resting EEG of male tinnitus patients (n = 8, mean age 54 years) were compared to those of age-matched healthy males (n = 15, mean age 58.8 years). On average, the patient group exhibited higher spectral power over the frequency range of 2-100 Hz. Using LORETA source analysis, the generators of delta, theta, alpha and beta power increases were localized dominantly to left auditory (Brodmann Areas (BA) 41,42, 22), temporo-parietal, insular posterior, cingulate anterior and parahippocampal cortical areas.</p> <p>Conclusions</p> <p>Tinnitus patients show a deviation from the norm of different resting EEG parameters, characterized by an overproduction of resting state delta, theta and beta brain activities, providing further support for the microphysiological and magnetoencephalographic evidence pointing to a thalamocortical dysrhythmic process at the source of tinnitus. These results also provide further confirmation that reciprocal involvements of both auditory and associative/paralimbic areas are essential in the generation of tinnitus.</p

The Effect of Low-Frequency Sound Stimulation on Patients with Fibromyalgia: A Clinical Study

Background: The search for effective treatments for fibromyalgia (FM) has continued for years. The present study premises that thalamocortical dysrhythmia is implicated in fibromyalgia and that low-frequency sound stimulation (LFSS) can play a regulatory function by driving neural rhythmic oscillatory activity. Objective: To assess the effect of LFSS on FM. Method: The present open-label study with no control group used a repeated-measures design with no noncompleters. Nineteen female volunteers (median age 51 years; median duration of FM 5.76 years) were administered 10 treatments (twice per week for five weeks). Treatments involved 23 min of LFSS at 40 Hz, delivered using transducers in a supine position. Measures (repeated before and after treatment) included the Fibromyalgia Impact Questionnaire, Jenkins Sleep Scale, Pain Disability Index, sitting and standing without pain (in minutes), cervical muscle range of motion and muscle tone. Mean percentages were calculated on end of treatment selfreports of improvement on pain, mood, insomnia and activities of daily living. Results: Significant improvements were observed with median scores: Fibromyalgia Impact Questionnaire, 81% (P\u3c0.0001); Jenkins Sleep Scale, 90% (P\u3c0.0001); and Pain Disability Index, 49.1% (P\u3c0.0001). Medication dose was reduced in 73.68% of patients and completely discontinued in 26.32%. Time sitting and standing without pain increased significantly (P\u3c0.0001). Cervical muscle range of motion increased from 25% to 75% (P=0.001), while muscle tone changed from hypertonic to normal (P=0.0002). Conclusion: In the present study, the LFSS treatment showed no adverse effects and patients receiving the LFSS treatment showed statistically and clinically relevant improvement. Further phase 2 and 3 trials are warranted. Key Words

Magnetoencephalography reveals increased slow-to-fast alpha power ratios in patients with chronic pain

INTRODUCTION: Objective disease markers are a key for diagnosis and personalized interventions. In chronic pain, such markers are still not available, and therapy relies on individual patients' reports. However, several pain studies have reported group-based differences in functional magnetic resonance imaging, electroencephalography, and magnetoencephalography (MEG). OBJECTIVES: We aimed to explore spectral differences in resting-state MEG brain signals between patients with chronic pain and pain-free controls and to characterize the cortical and subcortical regions involved. METHODS: We estimated power spectral density over 5 minutes of resting-state MEG recordings in patients with chronic pain and controls and derived 7 spectral features at the sensor and source levels: alpha peak frequency, alpha power ratio (power 7–9 Hz divided by power 9–11 Hz), and average power in theta, alpha, beta, low-gamma, and high-gamma bands. We performed nonparametric permutation t tests (false discovery rate corrected) to assess between-group differences in these 7 spectral features. RESULTS: Twenty-one patients with chronic pain and 25 controls were included. No significant group differences were found in alpha peak frequency or average power in any frequency band. The alpha power ratio was significantly higher (P < 0.05) in patients with chronic pain at both the sensor and brain source levels. The brain regions showing significantly higher ratios included the occipital, parietal, temporal and frontal lobe areas, insular and cingulate cortex, and right thalamus. CONCLUSION: The alpha power ratio is a simple, promising signal marker of chronic pain, affecting an expansive range of cortical and subcortical regions, including known pain-processing areas