Preserved dynamic cerebral autoregulation in the middle cerebral artery among persons with migraine

Migraine affects the autonomous nervous system and a recent investigation has also proposed a severe disturbance of dynamic cerebral blood flow regulation in the middle cerebral artery during spontaneous blood pressure oscillations. This study investigates whether dynamic cerebral autoregulation is impaired in persons with migraine among a normal cohort. Out of 94 adults studied to establish normal values for dynamic autoregulation, 19 suffered from migraine according to IHS criteria (10 of them with aura). Transcranial Doppler sonography and fingerplethysmography were used to determine dynamic autoregulation of both middle cerebral arteries following spontaneous low frequency (0.06–0.12 Hz) blood pressure fluctuations (phase and gain of transfer function, correlation coefficient indices Dx and Mx). No significant differences were found for the low frequency variability of blood pressure (power spectral density) and various indices of dynamic cerebral autoregulation between persons with and without migraine. Moreover, no differences were observed between persons with migraine, with and without aura. This study based on a normal cohort does not support the presence of generally impaired cerebral autoregulation dynamics in persons with migraine. Future studies should focus on posterior circulation and particular cerebellar autoregulation.     

Cerebral autoregulation is compromised during simulated fluctuations in gravitational stress

Gravity places considerable stress on the cardiovascular system but cerebral autoregulation usually protects the cerebral blood vessels from fluctuations in blood pressure. However, in conditions such as those encountered on board a high-performance aircraft, the gravitational stress is constantly changing and might compromise cerebral autoregulation. In this study we assessed the effect of oscillating orthostatic stress on cerebral autoregulation. Sixteen (eight male) healthy subjects [aged 27 (1) years] were exposed to steady-state lower body negative pressure (LBNP) at –15 and –40 mmHg and then to oscillating LBNP at the same pressures. The oscillatory LBNP was applied at 0.1 and 0.2 Hz. We made continuous recordings of RR-interval, blood pressure, cerebral blood flow velocity (CBFV), respiratory frequency and end-tidal CO₂. Oscillations in mean arterial pressure (MAP) and CBFV were assessed by autoregressive spectral analysis. Respiration was paced at 0.25 Hz to avoid interference from breathing. Steady-state LBNP at –40 mmHg significantly increased low-frequency (LF, 0.03–0.14 Hz) powers of MAP (P<0.01) but not of CBFV. Oscillatory 0.1 Hz LBNP (0 to –40 mmHg) significantly increased the LF power of MAP to a similar level as steady-state LBNP but also resulted in a significant increase in the LF power of CBFV (P<0.01). Oscillatory LBNP at 0.2 Hz induced oscillations in MAP and CBFV at 0.2 Hz. Cross-spectral analysis showed that the transfer of LBNP-induced oscillations in MAP onto the CBFV was significantly greater at 0.2 Hz than at 0.1 Hz (P<0.01). These results show that the ability of the cerebral vessels to modulate fluctuations in blood pressure is compromised during oscillatory compared with constant gravitational stress. Furthermore, this effect seems to be more pronounced at higher frequencies of oscillatory stress.     

Dynamic pressure–flow relationship of the cerebral circulation during acute increase in arterial pressure

The physiological mechanism(s) for the regulation of the dynamic pressure–flow relationship of the cerebral circulation are not well understood. We studied the effects of acute cerebral vasoconstriction on the transfer function between spontaneous changes in blood pressure (BP) and cerebral blood flow velocity (CBFV) in 13 healthy subjects (30 ± 7 years). CBFV was measured in the middle cerebral artery using transcranial Doppler. BP was increased stepwise with phenylephrine infusion at 0.5, 1.0 and 2.0 μg kg^–1 min^–1. Phenylephrine increased BP by 11, 23 and 37% from baseline, while CBFV increased (11%) only with the highest increase in BP. Cerebrovascular resistance index (BP/CBFV) increased progressively by 6, 17 and 23%, demonstrating effective steady-state autoregulation. Transfer function gain at the low frequencies (LF, 0.07–0.20 Hz) was reduced by 15, 14 and 14%, while the phase was reduced by 10, 17 and 31%. A similar trend of changes was observed at the high frequencies (HF, 0.20–0.35 Hz), but gain and phase remained unchanged at the very low frequencies (VLF, 0.02–0.07 Hz). Windkessel model simulation suggests that increases in steady-state cerebrovascular resistance and/or decreases in vascular compliance during cerebral vasoconstriction contribute to the changes in gain and phase. These findings suggest that changes in steady-state cerebrovascular resistance and/or vascular compliance modulate the dynamic pressure–flow relationship at the low and high frequencies, while dynamic autoregulation is likely to be dominant at the very low frequencies. Thus, oscillations in CBFV are modulated not only by dynamic autoregulation, but also by changes in steady-state cerebrovascular resistance and/or vascular compliance.     

Rapid pressure-to-flow dynamics of cerebral autoregulation induced by instantaneous changes of arterial CO2

Continuous assessment of CA is desirable in a number of clinical conditions, where cerebral hemodynamics may change within relatively short periods. In this work, we propose a novel method that can improve temporal resolution when assessing the pressure-to-flow dynamics in the presence of rapid changes in arterial CO₂. A time-varying multivariate model is proposed to adaptively suppress the instantaneous effect of CO₂ on CBFV by the recursive least square (RLS) method. Autoregulation is then quantified from the phase difference (PD) between arterial blood pressure (ABP) and CBFV by calculating the instantaneous PD between the signals using the Hilbert transform (HT). A Gaussian filter is used prior to HT in order to optimize the temporal and frequency resolution and show the rapid dynamics of cerebral autoregulation. In 13 healthy adult volunteers, rapid changes of arterial CO₂ were induced by rebreathing expired air, while simultaneously and continuously recording ABP, CBFV and end-tidal CO₂ (ETCO₂). Both simulation and physiological studies show that the proposed method can reduce the transient distortion of the instantaneous phase dynamics caused by the effect of CO₂ and is faster than our previous method in tracking time-varying autoregulation. The normalized mean square error (NMSE) of the predicted CBFV can be reduced significantly by 38.7% and 37.7% (p < 0.001) without and with the Gaussian filter applied, respectively, when compared with the previous univariate model. These findings suggest that the proposed method is suitable to track rapid dynamics of cerebral autoregulation despite the influence of confounding covariates.     

Cerebral haemodynamics during the Mueller manoeuvre in humans.

Voluntary negative intra-thoracic pressure (Mueller manoeuvre) is known to reduce arterial blood pressure (ABP). To investigate changes in cerebral blood flow velocity (CBFV) during 15 s Mueller manoeuvres at -30 mmHg intra-thoracic pressure, 27 young (aged 21-31 years, group A) and 11 older (52-64 years, group B) healthy adults were studied using transcranial Doppler and non-invasive ABP measurement (Finapres). After closely following the initial ABP drop, CBFV showed an overshoot during temporary recovery of ABP. Then ABP and CBFV decreased significantly to below baseline. While ABP declined further until the end of the manoeuvre, CBFV increased in group A 4.7 s (2.4-8.5) (median and range) and in group B 5.7 s (4. 1-7.2) after the onset of the CBFV decrease. Critical closing pressure (CCP), calculated for each cardiac cycle from the dynamic pressure-flow relationship (DPFR), indicated a reduction of intra-cranial pressure during the first half of the strain. DPFR-related estimation of cerebrovascular resistance provided a more physiological response than the conventional cerebrovascular resistance quotient ABP/CBFV, and decreased about 1.5 s before the observed CBFV increase. A modification of the previously described dynamic auto-regulation index ROR correlated significantly with CO2 reactivity values (r=0.61, P=0.001). In conclusion, changes in CBFV during Mueller manoeuvres are likely to reflect dynamic cerebral auto-regulation and may provide an estimate of dynamic cerebral auto-regulation capacity. In older adults, the maximal dynamic auto-regulatory response seems to be unchanged, but the onset of reaction is slightly delayed.     

Analysis of dynamic cerebral autoregulation using an ARX model based on arterial blood pressure and middle cerebral artery velocity simulation

The study aimed to model the cerebrovascular system, using a linear ARX model based on data simulated by a comprehensive physiological model, and to assess the range of applicability of linear parametric models. Arterial blood pressure (ABP) and middle cerebral arterial blood flow velocity (MCAV) were measured from 11 subjects non-invasively, following step changes in ABP, using the thigh cuff technique. By optimising parameters associated with autoregulation, using a non-linear optimisation technique, the physiological model showed a good performance (r=0.83±0.14) in fitting MCAV. An additional five sets of measured ABP of length 236±154 s were acquired from a subject at rest. These were normalised and rescaled to coefficients of variation (CV=SD/mean) of 2% and 10% for model comparisons. Randomly generated Gaussian noise with standard deviation (SD) from 1% to 5% was added to both ABP and physiologically simulated MCAV (SMCAV), with ‘normal’ and ‘impaired’ cerebral autoregulation, to simulate the real measurement conditions. ABP and SMCAV were fitted by ARX modelling, and cerebral autoregulation was quantified by a 5 s recovery percentage R5% of the step responses of the ARX models. The study suggests that cerebral autoregulation can be assessed by computing the R5% of the step response of an ARX model of appropriate order, even when measurement noise is considerable.     

Oscillations in cerebral blood flow and cortical oxygenation in Alzheimer's disease

In Alzheimer's disease (AD) cerebrovascular function is at risk. Transcranial Doppler, near-infrared spectroscopy, and photoplethysmography are noninvasive methods to continuously measure changes in cerebral blood flow velocity (CBFV), cerebral cortical oxygenated hemoglobin (O₂Hb), and blood pressure (BP). In 21 patients with mild to moderate AD and 20 age-matched controls, we investigated how oscillations in cerebral blood flow velocity (CBFV) and O₂Hb are associated with spontaneous and induced oscillations in blood pressure (BP) at the very low (VLF = 0.05 Hz) and low frequencies (LF = 0.1 Hz). We applied spectral and transfer function analysis to quantify dynamic cerebral autoregulation and brain tissue oxygenation. In AD, cerebrovascular resistance was substantially higher (34%, AD vs. control: Δ = 0.69 (0.25) mm Hg/cm/second, p = 0.012) and the transmission of very low frequency (VLF) cerebral blood flow (CBF) oscillations into O₂Hb differed, with increased phase lag and gain (Δ phase 0.32 [0.15] rad; Δ gain 0.049 [0.014] μmol/cm/second, p both < 0.05). The altered transfer of CBF to cortical oxygenation in AD indicates that properties of the cerebral microvasculature are changed in this disease.     

Neural network modelling of dynamic cerebral autoregulation: assessment and comparison with established methods

A time lagged recurrent neural network (TLRN) was implemented to model the dynamic relationship between arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) and its performance was compared to classical linear model such as transfer function analysis, Aaslid's dynamic autoregulation model, and the Wiener-Laguerre moving average filter. A simple linear regression was also tested as a naive estimator. In 16 normal subjects, CBFV was continuously recorded with Doppler ultrasound and ABP with the Finapres device during six repeated thigh cuff manoeuvres. Using mean beat-to-beat values of ABP as input and CBFV as output, the performance of each method was assessed by the model's predicted velocity correlation coefficient and normalized mean square error (MSE). Cross-validation was performed using three thigh cuff manoeuvres for the training data set and the other three for the validation set. The four methods studied performed significantly better than the zero-order naive estimator. The TLRN performed better than transfer function analysis, but was not significantly different from the time-domain techniques, despite showing the minimum predictive MSE. CBFV step responses could be extracted from the TLRN showing the presence of non-linear behaviour both in terms of amplitude and directionality.     

Evaluation of impaired dynamic cerebral autoregulation by the Mueller manoeuvre.

Arterial blood pressure (ABP) shows polyphasic changes during the Mueller manoeuvre (voluntary negative intrathoracic pressure). The aim of the present study was to investigate (1) whether these changes could be applied to detect impaired dynamic cerebral autoregulation (dCA) in carotid stenosis and (2) whether the degree of indicated impairment correlates with transfer function phase as another current measure for dCA (deep breathing method) and CO2-reactivity. We examined 13 patients with severe unilateral carotid artery stenosis and 16 age-matched controls during 15-s Mueller manoeuvres (MM) at -30 mmHg using bilateral transcranial Doppler sonography and non-invasive ABP recordings (Finapres, 2300, Ohmeda, Englewood, CO, USA). After an initial biphasic oscillation, cerebral blood flow velocity (CBFV) and ABP decreased to below baseline. CBFV reincreased in controls and on contralateral sides in patients 6.0 s (3.8-9.5 s, median and range) after the onset of the decrease, despite a further fall in ABP. CBFV over the affected side revealed a significantly delayed reincrease (8.0 (5.6-10.3) s; P<0.01) combined with a relatively flat and inertial amplitude behaviour. An applied autoregulation index derived from the MM (mROR), phase shift and CO2-reactivity were severely reduced on the affected side in patients (P<0.01). Reduction of the mROR correlated significantly with reduction of phase shift (r=0.69; P=0.002) and CO2-reactivity (r=0.78; P=0.002). In conclusion, the different cerebral haemodynamic pattern during the MM in patients is likely to reflect impaired dCA. The degree of indicated impairment correlates with that of transfer function phase and CO2-reactivity. Therefore, the MM represents a convenient method for grading of compromised cerebral haemodynamics in patients with carotid artery stenosis.     

A Parametric Approach to Measuring Cerebral Blood Flow Autoregulation from Spontaneous Variations in Blood Pressure

Autoregulation maintains cerebral blood flow (CBF) almost constant in the face of changes in arterial blood pressure (ABP). Tests for impairment of this process using only spontaneous fluctuations in ABP, without provoking large variations, are of great clinical interest, and a range of different approaches have previously been applied. Extending earlier work based on linear filters, we propose a simple parametric method using a first order finite impulse response filter. We evaluate the method on ABP and CBF velocity [(CBFV), from trancranial Doppler ultrasound] signals collected in 60 patients with stenosis or occlusion of the carotid arteries. Data were collected during the inspiration of ambient air, a 5% CO2/air mixture, and finally the return to ambient air. Equivalent data were collected in 15 normal subjects. The filters estimated from the data segments with constant inspiratory pCO2 showed the expected high-pass characteristic, which was reduced during hypercapnia and also in patients. Highly significant correlation between the filter parameters and cerebrovascular reactivity (percent increase in CBFV per unit change in end-tidal pCO2) gives further evidence that the filters reflect autoregulation. The method allows simple parametrization of the dynamic autoregulatory responses in CBFV, and the analysis of short (1 min) data segments. © 2001 Biomedical Engineering Society. PAC01: 8719Uv, 4762+q, 4380Qf     

Visually evoked blood flow responses and interaction with dynamic cerebral autoregulation: Correction for blood pressure variation

Visually evoked flow responses recorded using transcranial Doppler ultrasonography are often quantified using a dynamic model of neurovascular coupling. The evoked flow response is seen as the model's response to a visual step input stimulus. However, the continuously active process of dynamic cerebral autoregulation (dCA) compensating cerebral blood flow for blood pressure fluctuations may induce changes of cerebral blood flow velocity (CBFV) as well. The effect of blood pressure variability on the flow response is evaluated by separately modeling the dCA-induced effects of beat-to-beat measured blood pressure related CBFV changes.Parameters of 71 subjects are estimated using an existing, well-known second order dynamic neurovascular coupling model proposed by Rosengarten et al. [1], and a new model extending the existing model with a CBFV contributing component as the output of a dCA model driven by blood pressure as input.Both models were evaluated for mean and systolic CBFV responses. The model-to-data fit errors of mean and systolic blood pressure for the new model were significantly lower compared to the existing model: mean: 0.8% ± 0.6 vs. 2.4% ± 2.8, p < 0.001; systolic: 1.5% ± 1.2 vs. 2.2% ± 2.6, p < 0.001. The confidence bounds of all estimated neurovascular coupling model parameters were significantly (p < 0.005) narrowed for the new model.In conclusion, blood pressure correction of visual evoked flow responses by including cerebral autoregulation in model fitting of averaged responses results in significantly lower fit errors and by that in more reliable model parameter estimation. Blood pressure correction is more effective when mean instead of systolic CBFV responses are used. Measurement and quantification of neurovascular coupling should include beat-to-beat blood pressure measurement.     

Reproducibility and variability of dynamic cerebral autoregulation during passive cyclic leg raising

Dynamic cerebral autoregulation (dCA) estimates require mean arterial blood pressure (MABP) fluctuations of sufficient amplitude. Current methods to induce fluctuations are not easily implemented or require patient cooperation. In search of an alternative method, we evaluated if MABP fluctuations could be increased by passive cyclic leg raising (LR) and tested if reproducibility and variability of dCA parameters could be improved.Middle cerebral artery cerebral blood flow velocity (CBFV), MABP and end tidal CO₂ (PetCO₂) were obtained at rest and during LR at 0.1 Hz in 16 healthy subjects. The MABP–CBFV phase difference and gain were determined at 0.1 Hz and in the low frequency (LF) range (0.06–0.14 Hz). In addition the autoregulation index (ARI) was calculated.The LR maneuver increased the power of MABP fluctuations at 0.1 Hz and across the LF range. Despite a clear correlation between both phase and gain reproducibility and MABP variability in the rest condition, only the reproducibility of gain increased significantly with the maneuver. During the maneuver patients were breathing faster and more irregularly, accompanied by increased PetCO₂ fluctuations and increased coherence between PetCO₂ and CBFV. Multiple regression analysis showed that these concomitant changes were negatively correlated with the MABP–CBFV phase difference at 0.1 Hz Variability was not reduced by LR for any of the dCA parameters.The clinical utility of cyclic passive leg raising is limited because of the concomitant changes in PetCO₂. This limits reproducibility of the most important dCA parameters. Future research on reproducibility and variability of dCA parameters should incorporate PetCO₂ variability or find methods to keep PetCO₂ levels constant.     

Estimating normal and pathological dynamic responses in cerebral blood flow velocity to step changes in end-tidal pCO2

The regulation of cerebral blood flow (CBF) following changes in arterial blood pressure (ABP) and end-tidal pCO₂ (EtCO₂) are of clinical interest in assessing cerebrovascular reserve capacity. Linear finite-impulse-response modelling is applied to ABP, EtCO₂ and CBF velocity (CBFV, from transcranial Doppler measurements), which allows the CBFV response to ideal step changes in EtCO₂ to be estimated from clinical data showing more sluggish, and additional random variations. The confounding effects of ABP changes provoked by hypercapnia on the CBFV are also corrected for. Data from 56 patients suffering from stenosis of the carotid arteries (with normal or diminished cerebrovascular reactivity to EtCO₂ changes—CVR_{CO 2} were analysed. The results show the expected significant differences (p<0.05) between EtCO₂ steps up and down, the significant contribution from ABP variation, and also differences in the dynamic responses of patients with reduced CVR_{CO 2} (p<0.01 after 10 s). For the latter the CBFV response appears exhausted after about 15s, whereas for normals CBFV continues to increase. While dispersion of individual step responses remains large, the method gives encouraging results for the non-invasive study of compromised haemodynamics in different patient groups.     

Dynamic cerebral autoregulation assessment using an ARX model: comparative study using step response and phase shift analysis

Middle cerebral arterial blood velocity (MCAv) response to spontaneous and manipulated changes of arterial blood pressure (ABP) was studied in eight subjects using a linear autoregressive with exogenous input (ARX) model. ABP and MCAv were measured non-invasively by photoplethysmograph and transcranial Doppler ultrasound, respectively. Data were recorded at rest (spontaneous changes in ABP) and during thigh cuff (step-wise changes) and lower body negative pressure (sinusoidal changes of 1/12 Hz) tests in both normocapnia and hypercapnia (5% CO2). Since autoregulation is modulated by CO2, respiratory CO2 was simultaneously monitored to allow comparison of cerebral autoregulation status with different CO2 levels. ABP and MCAv were fitted by ARX models and dynamic cerebral autoregulation was estimated by analysing both the step responses and phase shift at the 1/12 Hz of the corresponding ARX models. The ARX model consistently modelled the phase lead of MCAv to ABP and it showed that the phase shift at 1/12 Hz of ARX model is consistent with the real phase shift of the data (p=0.59). Strong linear relationships between pCO2 and gradient of the step response (r=-0.58, p<0.0001) and between pCO2 and phase shift (r=-0.76, p<0.0001) were observed, which suggests that cerebral autoregulation can be assessed by step response or phase shift analysis of the ARX model fitted to ABP and MCAv data with spontaneous changes.     

Modeling of nonlinear physiological systems with fast and slow dynamics. II. Application to cerebral autoregulation

Dynamic autoregulation of cerebral hemodynamics in healthy humans is studied using the novel methodology of the Laguerre–Volterra network for systems with fast and slow dynamics (Mitsis, G. D., and V. Z. Marmarelis, Ann. Biomed. Eng. 30:272–281, 2002). Since cerebral autoregulation is mediated by various physiological mechanisms with significantly different time constants, it is used to demonstrate the efficacy of the new method. Results are presented in the time and frequency domains and reveal that cerebral autoregulation is a nonlinear and dynamic (frequency-dependent) system with considerable nonstationarities. Quantification of the latter reveals greater variability in specific frequency bands for each subject in the low and middle frequency range (below 0.1 Hz). The nonlinear dynamics are prominent also in the low and middle frequency ranges, where the frequency response of the system exhibits reduced gain. © 2002 Biomedical Engineering Society. PAC2002: 8719Uv, 8719La, 8710+e     

Effects of Autoregulation and CO<Subscript>2</Subscript> Reactivity on Cerebral Oxygen Transport

Both autoregulation and CO₂ reactivity are known to have significant effects on cerebral blood flow and thus on the transport of oxygen through the vasculature. In this paper, a previous model of the autoregulation of blood flow in the cerebral vasculature is expanded to include the dynamic behavior of oxygen transport through binding with hemoglobin. The model is used to predict the transfer functions for both oxyhemoglobin and deoxyhemoglobin in response to fluctuations in arterial blood pressure and arterial CO₂ concentration. It is shown that only six additional nondimensional groups are required in addition to the five that were previously found to characterize the cerebral blood flow response. A resonant frequency in the pressure-oxyhemoglobin transfer function is found to occur in the region of 0.1 Hz, which is a frequency of considerable physiological interest. The model predictions are compared with results from the published literature of phase angle at this frequency, showing that the effects of changes in breathing rate can significantly alter the inferred phase dynamics between blood pressure and hemoglobin. The question of whether dynamic cerebral autoregulation is affected under conditions of stenosis or stroke is then examined.     

Optimising the assessment of cerebral autoregulation from black box models

Cerebral autoregulation (CA) mechanisms maintain blood flow approximately stable despite changes in arterial blood pressure. Mathematical models that characterise this system have been used extensively in the quantitative assessment of function/impairment of CA. Using spontaneous fluctuations in arterial blood pressure (ABP) as input and cerebral blood flow velocity (CBFV) as output, the autoregulatory mechanism can be modelled using linear and non-linear approaches, from which indexes can be extracted to provide an overall assessment of CA. Previous studies have considered a single – or at most a couple of measures, making it difficult to compare the performance of different CA parameters. We compare the performance of established autoregulatory parameters and propose novel measures. The key objective is to identify which model and index can best distinguish between normal and impaired CA. To this end 26 recordings of ABP and CBFV from normocapnia and hypercapnia (which temporarily impairs CA) in 13 healthy adults were analysed. In the absence of a ‘gold’ standard for the study of dynamic CA, lower inter- and intra-subject variability of the parameters in relation to the difference between normo- and hypercapnia were considered as criteria for identifying improved measures of CA. Significantly improved performance compared to some conventional approaches was achieved, with the simplest method emerging as probably the most promising for future studies.     

The role of adenosine in autoregulation of cerebral blood flow

We have investigated the role of adenosine, a purine nucleoside and potent vasodilator of cerebral pial vessels, during both acute (0–60 sec) and sustained (2–5 min) changes in cerebral perfusion pressure. Brain adenosine concentrations are rapidly increased within 5 sec of the onset of systemic hypotension and parallel, in a temporal fashion, the changes in pial vessel diameter and alterations in cerebral vascular resistance. During sustained hypotension, brain levels of adenosine are increased even within the autoregulatory range. These data are constant with the hypothesis that adenosine is an important metabolic factor in cerebral autoregulation.     

Temporal dynamics of primary motor cortex γ oscillation amplitude and piper corticomuscular coherence changes during motor control

In recent years, the use of non-invasive techniques (EEG/MEG) to measure the ~80 Hz (“gamma”) oscillations generated by the primary motor cortex during motor control has been well validated. However, primary motor cortex gamma oscillations have yet to be systematically compared with lower frequency (30–50 Hz, ‘piper’) corticomuscular coherence in the same tasks. In this paper, primary cortex gamma oscillations and piper corticomuscular coherence are compared for three types of movements: simple abductions of the index finger, repetitive abductions of the index finger of different extents and frequencies and static abduction of the index finger at two different force levels. For simple movements, piper coherence and gamma amplitude followed very similar time courses with coherence appearing at approximately half the frequency of cortical gamma oscillations. No evidence of 2:1 phase–phase coupling was observed. A similar pattern of results was observed for repetitive movements varying in size and frequency; however, during the production of static force, the time courses became dissociated. During these movements, EMG piper amplitude was sustained for the entire contraction; gamma power showed a burst at onset but no piper corticomuscular coherence was observed. For these data, this dissociation suggests that while primary motor cortex gamma oscillations and piper corticomuscular coherence may often co-occur during the production of dynamic movements, they probably reflect different functional processes in motor control.     

Fatigue related changes in electromyographic coherence between synergistic hand muscles

The aim of this study was to examine coherence between surface electromyographic (EMG) signals from two index finger flexor muscles, the first dorsal interosseous (FDI) and flexor digitorum superficialis (FDS), during and immediately following sustained, fatiguing isometric contraction. Coherence was observed between the FDI and FDS EMG signals in the tremor (8–12 Hz), beta (15–35 Hz) and gamma (35–60 Hz) bands in all subjects. A significant increase in EMG–EMG coherence in the beta and gamma frequency bands was observed immediately following the fatiguing contraction. No significant difference was observed in the tremor band coherence before and after fatigue. Coherence was observed between EMG and force in the tremor band during both the pre- and post-fatigue contractions and a significant increase in the FDI EMG-force coherence post-fatigue was observed. It is suggested that the increase in beta and gamma band coherence with fatigue may be due to increased levels of corticomotoneuronal drive to both muscles. Alternatively, the increased EMG–EMG coherence may reflect an increased contribution of peripheral afferents to coupling across the muscle with fatigue. Although the functional significance is not clear, the increase in coherence may help to overcome reduced motoneuron excitability with fatigue, to bind together different sensorimotor elements or to coordinate force generation across muscles in a more synergistic manner as the force generating capacity of the muscle is decreased.