The maternal brain is more flexible and responsive at rest: effective connectivity of the parental caregiving network in postpartum mothers.

The field of neuroscience has largely overlooked the impact of motherhood on brain function outside the context of responses to infant stimuli. Here, we apply spectral dynamic causal modelling (spDCM) to resting-state fMRI data to investigate differences in brain function between a group of 40 first-time mothers at 1-year postpartum and 39 age- and education-matched women who have never been pregnant. Using spDCM, we investigate the directionality (top-down vs. bottom-up) and valence (inhibition vs excitation) of functional connections between six key left hemisphere brain regions implicated in motherhood: the dorsomedial prefrontal cortex, ventromedial prefrontal cortex, posterior cingulate cortex, parahippocampal gyrus, amygdala, and nucleus accumbens. We show a selective modulation of inhibitory pathways related to differences between (1) mothers and non-mothers, (2) the interactions between group and cognitive performance and (3) group and social cognition, and (4) differences related to maternal caregiving behaviour. Across analyses, we show consistent disinhibition between cognitive and affective regions suggesting more efficient, flexible, and responsive behaviour, subserving cognitive performance, social cognition, and maternal caregiving. Together our results support the interpretation of these key regions as constituting a parental caregiving network. The nucleus accumbens and the parahippocampal gyrus emerging as 'hub' regions of this network, highlighting the global importance of the affective limbic network for maternal caregiving, social cognition, and cognitive performance in the postpartum period.

Resting state functional connectivity in adolescent synthetic cannabinoid users with and without attention-deficit/hyperactivity disorder.

OBJECTIVE: Synthetic cannabinoids (SCs) have become increasingly popular in recent years, especially among adolescents. The first aim of the current study was to examine resting-state functional connectivity (rsFC) in SC users compared to controls. Our second aim was to examine the influence of comorbid attention-deficit/hyperactivity disorder (ADHD) symptomatology on rsFC changes in SC users compared to controls. METHODS: Resting-state functional magnetic resonance imaging (fMRI) analysis included 25 SC users (14 without ADHD and 11 with ADHD combined type) and 12 control subjects. RESULTS: We found (i) higher rsFC between the default mode network (DMN) and salience network, dorsal attention network and cingulo-opercular network, and (ii) lower rsFC within the DMN and between the DMN and visual network in SC users compared to controls. There were no significant differences between SC users with ADHD and controls, nor were there any significant differences between SC users with and without ADHD. CONCLUSIONS: We found the first evidence of abnormalities within and between resting state networks in adolescent SC users without ADHD. In contrast, SC users with ADHD showed no differences compared to controls. These results suggest that comorbidity of ADHD and substance dependence may show different rsFC alterations than substance use alone.

Aberrant plasticity in musculoskeletal pain: a failure of homeostatic control?

Aberrant synaptic plasticity is hypothesised to underpin chronic pain. Yet, synaptic plasticity regulated by homeostatic mechanisms have received limited attention in pain. We investigated homeostatic plasticity in the human primary motor cortex (M1) of 21 healthy individuals in response to experimentally induced muscle pain for several days. Experimental pain was induced by injecting nerve growth factor into the muscle belly of the right extensor carpi radialis brevis muscle. Pain and disability were monitored until day 21. Homeostatic plasticity was induced on day 0, 2, 4, 6, and 14 in the left M1 using anodal transcranial direct stimulation (tDCS) applied for 7 and 5 min, separated by a 3-min rest period. Motor-evoked potentials (MEP) to transcranial magnetic stimulation assessed the homeostatic response. On days 0 and 14, MEPs increased following the first block of tDCS (p < 0.004), and decreased following the second block of tDCS (p < 0.001), consistent with a normal homeostatic response. However, on days 2 (p = 0.07) and 4 (p = 0.7), the decrease in MEPs after the second block of tDCS was attenuated, representing an impaired homeostatic response. Findings demonstrate altered homeostatic plasticity in the M1 with the greatest alteration observed after 4 days of sustained pain. This study provides longitudinal insight into homeostatic plasticity in response to the development, maintenance, and resolution of pain over the course of 14 days.

Neural multimodal integration underlying synchronization with a co-performer in music: Influences of motor expertise and visual information.

Sensorimotor synchronization is a general skill that musicians have developed to the highest levels of performance, including synchronization in timing and articulation. This study investigated neurocognitive processes that enable such high levels of performance, specifically testing the relevance of 1) motor resonance and sharing high levels of motor expertise with the co-performer, and 2) the role of visual information in addition to auditory information. Musicians with varying levels of piano expertise (including non-pianists) performed on a single piano key with their right hand along with recordings of a pianist who performed simple melodies with the left hand, synchronizing timing and articulation. The prerecorded performances were presented as audio-only, audio-video, or audio-animation stimuli. Double pulse Transcranial Magnetic Stimulation (dTMS) was applied to test the contribution of the right dorsal premotor cortex (dPMC), an area implicated in motor resonance with observed (left-hand) actions, and the contribution of the right intraparietal sulcus (IPS), an area known for multisensory binding. Results showed effects of dTMS in the conditions that included visual information. IPS stimulation improved synchronization, although this effect was found to reverse in the video condition with higher levels of piano expertise. dPMC stimulation improved or worsened synchronization ability. Level of piano expertise was found to influence this direction in the video condition. These results indicate that high levels of relevant motor expertise are required to beneficially employ visual and motor information of a co-performer for sensorimotor synchronization, which may qualify the effects of dPMC and IPS involvement.

Cerebral peak alpha frequency reflects average pain severity in a human model of sustained, musculoskeletal pain.

Heightened pain sensitivity, the amount of pain experienced in response to a noxious event, is a known risk factor for development of chronic pain. We have previously reported that pain-free, sensorimotor peak alpha frequency (PAF) is a reliable biomarker of pain sensitivity for thermal, prolonged pains lasting tens of minutes. To test whether PAF can provide information about pain sensitivity occurring over clinically relevant timescales (i.e., weeks), EEG was recorded before and while participants experienced a long-lasting pain model, repeated intramuscular injection of nerve growth factor (NGF), that produces progressively developing muscle pain for up to 21 days. We demonstrate that pain-free, sensorimotor PAF is negatively correlated with NGF pain sensitivity; increasingly slower PAF is associated with increasingly greater pain sensitivity. Furthermore, PAF remained stable following NGF injection, indicating that the presence of NGF pain for multiple weeks is not sufficient to induce the PAF slowing reported in chronic pain. In total, our results demonstrate that slower pain-free, sensorimotor PAF is associated with heightened sensitivity to a long-lasting musculoskeletal pain and also suggest that the apparent slowing of PAF in chronic pain may reflect predisease pain sensitivity.NEW & NOTEWORTHY Pain sensitivity, the intensity of pain experienced after injury, has been identified as an important risk factor in the development of chronic pain. Biomarkers of pain sensitivity have the potential to ease chronic pain burdens by preventing disease emergence. In the current study, we demonstrate that the speed of pain-free, sensorimotor peak alpha frequency recorded during resting-state EEG predicts pain sensitivity to a clinically-relevant, human model of prolonged pain that persists for weeks.

Corticomotor Depression is Associated With Higher Pain Severity in the Transition to Sustained Pain: A Longitudinal Exploratory Study of Individual Differences.

Aberrant motor cortex plasticity is hypothesized to contribute to chronic musculoskeletal pain, but evidence is limited. Critically, studies have not considered individual differences in motor plasticity or how this relates to pain susceptibility. Here we examined the relationship between corticomotor excitability and an individual's susceptibility to pain as pain developed, was sustained and resolved over 21 days. Nerve growth factor was injected into the right extensor carpi radialis brevis muscle of 20 healthy individuals on day 0, 2, and 4. Corticomotor excitability, pressure pain thresholds and performance on a cognitive conflict task were examined longitudinally (day 0, 2, 4, 6, and 14). Pain and disability were assessed on each alternate day (1,3…21). Two patterns of motor plasticity were observed in response to pain--corticomotor depression or corticomotor facilitation (P = .009). Individuals who displayed corticomotor depression experienced greater pain (P = .027), and had worse cognitive task performance (P = .038), than those who displayed facilitation. Pressure pain thresholds were reduced to a similar magnitude in both groups. Corticomotor depression in the early stage of pain could indicate a higher susceptibility to pain. Further work is required to determine whether corticomotor depression is a marker of pain susceptibility in musculoskeletal conditions. PERSPECTIVE: This article explores individual differences in motor plasticity in the transition to sustained pain. Individuals who developed corticomotor depression experienced higher pain and worse cognitive task performance than those who developed corticomotor facilitation. Corticomotor depression in the early stage of pain could indicate a higher susceptibility to pain.

The influence of kinesiology tape colour on performance and corticomotor activity in healthy adults: a randomised crossover controlled trial.

BACKGROUND: There exists conflicting evidence regarding the impact of kinesiology tape on performance and muscle function. One variable that may account for disparities in the findings of previous studies is the colour of the tape applied. Colour is hypothesised to influence sporting performance through modulation of arousal and aggression. However, few studies have investigated the influence of colour on products designed specifically to enhance athletic performance. Further, no studies have investigated the potential influence of colour on other drivers of performance, such as corticomotor activity and neuromuscular function. Thus, the aim of this study was to investigate the influence of kinesiology tape colour on athletic performance, knee extensor torque, and quadriceps neuromuscular function. METHODS: Thirty two healthy participants were assessed under five conditions, applied in random order: (1) no kinesiology tape (control), (2) beige-coloured kinesiology tape applied with tension (sham A), (3) beige-coloured kinesiology tape applied with no tension (sham B), (4) red-coloured kinesiology tape applied with tension, and (5) blue-coloured kinesiology tape applied with tension. Athletic performance was assessed using a previously validated hop test, knee extensor torque was measured using an isokinetic dynamometer, and transcranial magnetic stimulation was utilised to provide insight into the neuromuscular functioning of the quadriceps musculature. RESULTS: Kinesiology tape had no beneficial impact on lower limb performance or muscle strength in healthy adults. The colour of the tape did not influence athletic performance (F (4, 120) = 0.593, p = 0.669), quadriceps strength (F (4, 120) = 0.787, p = 0.536), or neuromuscular function (rectus femoris: F (2.661, 79.827) = 1.237, p = 0.301). CONCLUSION: This study found that kinesiology tape does not alter lower limb performance or muscle function in healthy adults, irrespective of the colour of the tape applied. Future research should seek to confirm these findings beyond the research setting, across a range of sports, and at a range of skill levels. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry. ACTRN12616001506482. Prospectively registered on 01/11/2016.

Test-Retest Reliability of Homeostatic Plasticity in the Human Primary Motor Cortex.

Homeostatic plasticity regulates synaptic activity by preventing uncontrolled increases (long-term potentiation) or decreases (long-term depression) in synaptic efficacy. Homeostatic plasticity can be induced and assessed in the human primary motor cortex (M1) using noninvasive brain stimulation. However, the reliability of this methodology has not been investigated. Here, we examined the test-retest reliability of homeostatic plasticity induced and assessed in M1 using noninvasive brain stimulation in ten, right-handed, healthy volunteers on days 0, 2, 7, and 14. Homeostatic plasticity was induced in the left M1 using two blocks of anodal transcranial direct current stimulation (tDCS) applied for 7 min and 5 min, separated by a 3 min interval. To assess homeostatic plasticity, 15 motor-evoked potentials to single-pulse transcranial magnetic stimulation were recorded at baseline, between the two blocks of anodal tDCS, and at 0 min, 10 min, and 20 min follow-up. Test-retest reliability was evaluated using intraclass correlation coefficients (ICCs). Moderate-to-good test-retest reliability was observed for the M1 homeostatic plasticity response at all follow-up time points (0 min, 10 min, and 20 min, ICC range: 0.43-0.67) at intervals up to 2 weeks. The greatest reliability was observed when the homeostatic response was assessed at 10 min follow-up (ICC > 0.61). These data suggest that M1 homeostatic plasticity can be reliably induced and assessed in healthy individuals using two blocks of anodal tDCS at intervals of 48 hours, 7 days, and 2 weeks.

Disruption of cortical synaptic homeostasis in individuals with chronic low back pain.

OBJECTIVE: Homeostatic plasticity mechanisms regulate synaptic plasticity in the human brain. Impaired homeostatic plasticity may contribute to maladaptive synaptic plasticity and symptom persistence in chronic musculoskeletal pain. METHODS: We examined homeostatic plasticity in fifty individuals with chronic low back pain (cLBP) and twenty-five pain-free controls. A single block (7-min) of anodal transcranial direct current stimulation ('single tDCS'), or two subsequent blocks (7-min and 5-min separated by 3-min rest; 'double tDCS'), were randomised across two experimental sessions to confirm an excitatory response to tDCS applied alone, and evaluate homeostatic plasticity, respectively. Corticomotor excitability was assessed in the corticomotor representation of the first dorsal interosseous muscle by transcranial magnetic stimulation-induced motor evoked potentials (MEPs) recorded before and 0, 10, 20, and 30-min following each tDCS protocol. RESULTS: Compared with baseline, MEP amplitudes increased at all time points in both groups following the single tDCS protocol (P < 0.003). Following the double tDCS protocol, MEP amplitudes decreased in pain-free controls at all time points compared with baseline (P < 0.01), and were unchanged in the cLBP group. CONCLUSION: These data indicate impaired homeostatic plasticity in the primary motor cortex of individuals with cLBP. SIGNIFICANCE: Impaired homeostatic plasticity could explain maladaptive synaptic plasticity and symptom persistence in cLBP.

The Response of the Primary Motor Cortex to Neuromodulation is Altered in Chronic Low Back Pain: A Preliminary Study.

Objective: Neuromodulation is increasingly investigated for the treatment of low back pain (LBP). However, the neurophysiological effects of common neuromodulatory techniques (anodal transcranial direct current stimulation [tDCS] and peripheral electrical stimulation [PES]) have not been investigated in people with chronic LBP. Here we aimed to compare the effect of three neuromodulatory protocols (anodal tDCS, high intensity PES, and a priming protocol of combined tDCS/PES) on primary motor cortex (M1) excitability in people with and without chronic LBP. Design: Cross-sectional. Setting: University laboratory. Participants: Ten individuals with chronic LBP and 10 pain-free controls. Methods: Participants received four interventions in random order across separate sessions: 1) anodal tDCS to M1 + PES to the back muscles; 2) tDCS + sham PES; 3) sham tDCS + PES; or 4) sham tDCS + sham PES. Motor cortical excitability (map volume, discrete map peaks, and cortical silent period [CSP]) was measured before and after each intervention. Results: Anodal tDCS increased M1 excitability (increased map volume and reduced CSP) in controls but had no effect in the LBP group. PES reduced M1 excitability in both groups. The combined tDCS + PES treatment increased M1 excitability in the LBP group but had no effect in controls. Conclusions: The neurophysiological response to common neuromodulatory treatments differs between people with and without LBP. This has relevance for the design and tailoring of neuromodulation in pain. Further, if the goal of treatment is to increase M1 excitability, a priming protocol (e.g., combined tDCS + PES) may be more effective than tDCS alone.

Movement Does Not Promote Recovery of Motor Output Following Acute Experimental Muscle Pain.

Objective: To examine the effect of motor activity on the magnitude and duration of altered corticomotor output following experimental muscle pain. Design: Experimental, pre-post test. Setting: University laboratory. Subjects: Twenty healthy individuals. Methods: Participants were randomly allocated to a Rest or Movement group. The Rest group sat quietly without moving for the duration of the experiment. The Movement group repeated a unimanual pattern of five sequential keystrokes as quickly and as accurately as possible immediately following the resolution of pain. Pain was induced into the right extensor carpi radialis brevis muscle by a bolus injection of 0.5 mL hypertonic saline. Corticomotor output was assessed as motor evoked potentials in response to transcranial magnetic stimulation before, immediately after, and at 10, 20, and 30 minutes following pain resolution. Pain intensity was recorded every 30 seconds using an 11-point numerical rating scale. Results: There was no difference in peak pain intensity (P < 0.09) or duration (P < 0.2) between groups. Corticomotor output was reduced in both groups (P < 0.002) at 10 minutes (P < 0.002), 20 minutes (P < 0.02), and 30 minutes (P < 0.037) following the resolution of pain relative to baseline. There was no difference between groups at any time point. Conclusions: Performance of motor activity immediately following the resolution of acute muscle pain did not alter the magnitude or duration of corticomotor depression. Understanding corticomotor depression in the postpain period and what factors promote recovery has relevance for clinical pain syndromes where ongoing motor dysfunction, in the absence of pain, may predispose to symptom persistence or recurrence.