Reproducibility of Rolandic beta rhythm modulation in MEG and EEG.

The Rolandic beta rhythm, at ∼20 Hz, is generated in the somatosensory and motor cortices and is modulated by motor activity and sensory stimuli, causing a short lasting suppression that is followed by a rebound of the beta rhythm. The rebound reflects inhibitory changes in the primary sensorimotor (SMI) cortex, and thus it has been used as a biomarker to follow the recovery of patients with acute stroke. The longitudinal stability of beta rhythm modulation is a prerequisite for its use in long-term follow-ups. We quantified the reproducibility of beta rhythm modulation in healthy subjects in a 1-year-longitudinal study both for MEG and EEG at T0, 1 month (T1-month, n = 8) and 1 year (T1-year, n = 19). The beta rhythm (13-25 Hz) was modulated by fixed tactile and proprioceptive stimulations of the index fingers. The relative peak strengths of beta suppression and rebound did not differ significantly between the sessions, and intersession reproducibility was good or excellent according to intraclass correlation-coefficient values (0.70-0.96) both in MEG and EEG. Our results indicate that the beta rhythm modulation to tactile and proprioceptive stimulation is well reproducible within 1 year. These results support the use of beta modulation as a biomarker in long-term follow-up studies, e.g., to quantify the functional state of the SMI cortex during rehabilitation and drug interventions in various neurological impairments.NEW & NOTEWORTHY The present study demonstrates that beta rhythm modulation is highly reproducible in a group of healthy subjects within a year. Hence, it can be reliably used as a biomarker in longitudinal follow-up studies in different neurological patient groups to reflect changes in the functional state of the sensorimotor cortex.

Comparing MEG and EEG in detecting the ~20-Hz rhythm modulation to tactile and proprioceptive stimulation.

Modulation of the ~20-Hz brain rhythm has been used to evaluate the functional state of the sensorimotor cortex both in healthy subjects and patients, such as stroke patients. The ~20-Hz brain rhythm can be detected by both magnetoencephalography (MEG) and electroencephalography (EEG), but the comparability of these methods has not been evaluated. Here, we compare these two methods in the evaluating of ~20-Hz activity modulation to somatosensory stimuli. Rhythmic ~20-Hz activity during separate tactile and proprioceptive stimulation of the right and left index finger was recorded simultaneously with MEG and EEG in twenty-four healthy participants. Both tactile and proprioceptive stimulus produced a clear suppression at 300-350 â€‹ms followed by a subsequent rebound at 700-900 â€‹ms after stimulus onset, detected at similar latencies both with MEG and EEG. The relative amplitudes of suppression and rebound correlated strongly between MEG and EEG recordings. However, the relative strength of suppression and rebound in the contralateral hemisphere (with respect to the stimulated hand) was significantly stronger in MEG than in EEG recordings. Our results indicate that MEG recordings produced signals with higher signal-to-noise ratio than EEG, favoring MEG as an optimal tool for studies evaluating sensorimotor cortical functions. However, the strong correlation between MEG and EEG results encourages the use of EEG when translating studies to clinical practice. The clear advantage of EEG is the availability of the method in hospitals and bed-side measurements at the acute phase.

Feasibility and reproducibility of electroencephalography-based corticokinematic coherence.

Corticokinematic coherence (CKC) is the phase coupling between limb kinematics and cortical neurophysiological signals, reflecting cortical processing of proprioceptive afference, and it is reproducible when estimated with magnetoencephalography (MEG). However, feasibility and reproducibility of CKC based on electroencephalography (EEG) is still unclear and is the primary object of the present report. Thirteen healthy right-handed volunteers (seven females, 21.7 ± 4.3 yr) participated in two combined MEG/EEG sessions 12.6 ± 1.3 mo apart. Participants' dominant and nondominant index finger was continuously moved at 3 Hz for 4 min separately using a pneumatic-movement actuator. Coherence was computed between finger acceleration and three derivations of EEG signals: 1) average reference, 2) bipolar derivations, and 3) surface Laplacian. CKC strength was defined as the peak coherence value at movement frequency. Intraclass-correlation coefficient values (0.74-0.93) indicated excellent intersession reproducibility for CKC strength for all derivations and moved fingers. CKC strength obtained with EEG was approximately two times lower compared with MEG, but the values were positively correlated across the participants. CKC strength was significantly (P < 0.01) higher for bipolar (session 1: 0.19 ± 0.09; session 2: 0.20 ± 0.10) and surface Laplacian (session 1: 0.22 ± 0.09; session 2: 0.21 ± 0.09) derivations than for the average reference (session 1: 0.10 ± 0.04; session 2: 0.11 ± 0.05). We demonstrated that CKC is a feasible and reproducible tool to monitor proprioception using EEG recordings, although the strength of CKC was twice lower for EEG compared with MEG. Laplacian and bipolar (CP3-C1/CP3-C3 and CP4-C2/C4-FC2) EEG derivation(s) are recommended for future research and clinical use of CKC method. NEW & NOTEWORTHY The most important message in this report is that the corticokinematic coherence (CKC) method is a feasible and reproducible tool to quantify, map, and follow cortical proprioceptive ("the movement sense") processing using EEG that is more widely available for CKC recordings than previously used magnetoencephalography designs, in basic research, but especially in clinical environments. We provide useful recommendations for optimal EEG derivations for cost-effective experimental designs, making it possible to scale up in sample size in future studies.

Reproducibility of corticokinematic coherence.

Corticokinematic coherence (CKC) between limb kinematics and magnetoencephalographic (MEG) signals reflects cortical processing of proprioceptive afference. However, it is unclear whether strength of CKC is reproducible across measurement sessions. We thus examined reproducibility of CKC in a follow-up study. Thirteen healthy right-handed volunteers (7 females, 21.7 ±â€¯4.3 yrs) were measured using MEG in two separate sessions 12.6 ±â€¯1.3 months apart. The participant was seated and relaxed while his/her dominant or non-dominant index finger was continuously moved at 3 Hz (4 min for each hand) using a pneumatic movement actuator. Finger kinematics were recorded with a 3-axis accelerometer. Coherence was computed between finger acceleration and MEG signals. CKC strength was defined as the peak coherence value at 3 Hz form a single sensor among 40 pre-selected Rolandic gradiometers contralateral to the movement. Pneumatic movement actuator provided stable proprioceptive stimuli and significant CKC responses peaking at the contralateral Rolandic sensors. In the group level, CKC strength did not differ between the sessions in dominant (Day-1 0.40 ±â€¯0.19 vs. Day-2 0.41 ±â€¯0.17) or non-dominant (0.35 ±â€¯0.16 vs. 0.36 ±â€¯0.17) hand, nor between the hands. Intraclass-correlation coefficient (ICC) values indicated excellent inter-session reproducibility for CKC strength for both dominant (0.86) and non-dominant (0.97) hand. However, some participants showed pronounced inter-session variability in CKC strength, but only for the dominant hand. CKC is a promising tool to study proprioception in long-term longitudinal studies in the group level to follow, e.g., integrity of cortical proprioceptive processing with motor functions after stroke.

Evidence for genetic regulation of the human parieto-occipital 10-Hz rhythmic activity.

Several functional and morphological brain measures are partly under genetic control. The identification of direct links between neuroimaging signals and corresponding genetic factors can reveal cellular-level mechanisms behind the measured macroscopic signals and contribute to the use of imaging signals as probes of genetic function. To uncover possible genetic determinants of the most prominent brain signal oscillation, the parieto-occipital 10-Hz alpha rhythm, we measured spontaneous brain activity with magnetoencephalography in 210 healthy siblings while the subjects were resting, with eyes closed and open. The reactivity of the alpha rhythm was quantified from the difference spectra between the two conditions. We focused on three measures: peak frequency, peak amplitude and the width of the main spectral peak. In accordance with earlier electroencephalography studies, spectral peak amplitude was highly heritable (h(2)  > 0.75). Variance component-based analysis of 28 000 single-nucleotide polymorphism markers revealed linkage for both the width and the amplitude of the spectral peak. The strongest linkage was detected for the width of the spectral peak over the left parieto-occipital cortex on chromosome 10 (LOD = 2.814, nominal P < 0.03). This genomic region contains several functionally plausible genes, including GRID1 and ATAD1 that regulate glutamate receptor channels mediating synaptic transmission, NRG3 with functions in brain development and HRT7 involved in the serotonergic system and circadian rhythm. Our data suggest that the alpha oscillation is in part genetically regulated, and that it may be possible to identify its regulators by genetic analyses on a realistically modest number of samples.

Altered excitation-inhibition balance in the primary sensorimotor cortex to proprioceptive hand stimulation in cerebral palsy.

OBJECTIVE: Our objective was to clarify the primary sensorimotor (SM1) cortex excitatory and inhibitory alterations in hemiplegic (HP) and diplegic (DP) cerebral palsy (CP) by quantifying SM1 cortex beta power suppression and rebound with magnetoencephalography (MEG). METHODS: MEG was recorded from 16 HP and 12 DP adolescents, and their 32 healthy controls during proprioceptive stimulation of the index fingers evoked by a movement actuator. The related beta power changes were computed with Temporal Spectral Evolution (TSE). Peak strengths of beta suppression and rebound were determined from representative channels over the SM1 cortex. RESULTS: Beta suppression was stronger contralateral to the stimulus and rebound was weaker ipsilateral to the stimulation in DP compared to controls. Beta modulation strengths did not differ significantly between HP and the control group. CONCLUSIONS: The emphasized beta suppression in DP suggests less efficient proprioceptive processing in the SM1 contralateral to the stimulation. Their weak rebound further indicates reduced intra- and/or interhemispheric cortical inhibition, which is a potential neuronal mechanism for their bilateral motor impairments. SIGNIFICANCE: The excitation-inhibition balance of the SM1 cortex related to proprioception is impaired in diplegic CP. Therefore, the cortical and behavioral proprioceptive deficits should be better diagnosed and considered to better target individualized effective rehabilitation in CP.

Genome-wide linkage analysis of human auditory cortical activation suggests distinct loci on chromosomes 2, 3, and 8.

Neural processes are explored through macroscopic neuroimaging and microscopic molecular measures, but the two levels remain primarily detached. The identification of direct links between the levels would facilitate use of imaging signals as probes of genetic function and, vice versa, access to molecular correlates of imaging measures. Neuroimaging patterns have been mapped for a few isolated genes, chosen based on their connection with a clinical disorder. Here we propose an approach that allows an unrestricted discovery of the genetic basis of a neuroimaging phenotype in the normal human brain. The essential components are a subject population that is composed of relatives and selection of a neuroimaging phenotype that is reproducible within an individual and similar between relatives but markedly variable across a population. Our present combined magnetoencephalography and genome-wide linkage study in 212 healthy siblings demonstrates that auditory cortical activation strength is highly heritable and, specifically in the right hemisphere, regulated oligogenically with linkages to chromosomes 2q37, 3p12, and 8q24. The identified regions delimit as candidate genes TRAPPC9, operating in neuronal differentiation, and ROBO1, regulating projections of thalamocortical axons. Identification of normal genetic variation underlying neurophysiological phenotypes offers a non-invasive platform for an in-depth, concerted capitalization of molecular and neuroimaging levels in exploring neural function.

The effect of alertness and attention on the modulation of the beta rhythm to tactile stimulation.

Beta rhythm modulation has been used as a biomarker to reflect the functional state of the sensorimotor cortex in both healthy subjects and patients. Here, the effect of reduced alertness and active attention to the stimulus on beta rhythm modulation was investigated. Beta rhythm modulation to tactile stimulation of the index finger was recorded simultaneously with MEG and EEG in 23 healthy subjects (mean 23, range 19-35 years). The temporal spectral evolution method was used to obtain the peak amplitudes of beta suppression and rebound in three different conditions (neutral, snooze, and attention). Neither snooze nor attention to the stimulus affected significantly the strength of beta suppression nor rebound, although a decrease in suppression and rebound strength was observed in some subjects with a more pronounced decrease of alertness. The reduction of alertness correlated with the decrease of suppression strength both in MEG (left hemisphere r = 0.49; right hemisphere r = 0.49, *p < 0.05) and EEG (left hemisphere r = 0.43; right hemisphere r = 0.72, **p < 0.01). The results indicate that primary sensorimotor cortex beta suppression and rebound are not sensitive to slightly reduced alertness nor active attention to the stimulus at a group level. Hence, tactile stimulus-induced beta modulation is a suitable tool for assessing the sensorimotor cortex function at a group level. However, subjects' alertness should be maintained high during recordings to minimize individual variability.