An exploration of homeostatic plasticity in musculoskeletal pain

The brain has a remarkable capacity to reorganise itself through life. When changes occur at a cellular level between neurons, this is known as synaptic plasticity. Synaptic plasticity has been proposed to be a key mechanism underpinning the learning and memory formation that occurs following afferent input (i.e., incoming stimuli from movement and sensation). However, synaptic plasticity in the human brain follows a positive loop cycle where incoming stimuli can lead to excessive synaptic strengthening (long-term potentiation; LTP) or weakening (long-term depression; LTD). To prevent overexpression of LTP or LTD, regulatory mechanisms termed ‘homeostatic plasticity’ promote stability during synaptic plasticity. A large body of evidence suggests that short- or long-term changes to synaptic plasticity takes place following afferent input. Similarly, evidence also suggests synaptic plasticity is altered in individuals experiencing incoming stimuli that are painful. However, no study has examined homeostatic plasticity during pain. Published studies that have examined homeostatic plasticity in individuals with pathology have been conducted in neurological conditions such as writer’s cramp, and chronic migraine. These studies provide preliminary evidence that impaired homeostatic plasticity is associated with altered synaptic plasticity with patients displaying abnormally high primary motor cortex (M1) excitability, altered cortical organisation, increased pain perception, and sensorimotor dysfunction. As altered synaptic plasticity and similar clinical features have been observed in individuals with chronic musculoskeletal pain, it is possible that homeostatic plasticity is impaired during pain. Thus, the broad goal of this thesis was to explore the effect of pain, using a clinical chronic musculoskeletal pain population and an experimental pain model, on homeostatic plasticity in the M1. To address this broad goal, three primary research studies were conducted

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

No evidence for changes in GABA concentration, functional connectivity, or working memory following continuous theta burst stimulation over dorsolateral prefrontal cortex

Continuous theta burst stimulation (cTBS) is thought to reduce cortical excitability and modulate functional connectivity, possibly by altering cortical inhibition at the site of stimulation. However, most evidence comes from the motor cortex and it remains unclear whether similar effects occur following stimulation over other brain regions. We assessed whether cTBS over left dorsolateral prefrontal cortex altered gamma aminobutyric acid (GABA) concentration, functional connectivity and brain dynamics at rest, and brain activation and memory performance during a working memory task. Seventeen healthy individuals participated in a randomised, sham-controlled, cross-over experiment. Before and after either real or sham cTBS, magnetic resonance spectroscopy was obtained at rest to measure GABA concentrations. Functional magnetic resonance imaging (fMRI) was also recorded at rest and during an n-back working memory task to measure functional connectivity, regional brain activity (low-frequency fluctuations), and task-related patterns of brain activity. We could not find evidence for changes in GABA concentration (P = 0.66, Bayes factor [BF10] = 0.07), resting-state functional connectivity (P(FWE) > 0.05), resting-state low-frequency fluctuations (P = 0.88, BF10 = 0.04), blood-oxygen level dependent activity during the n-back task (P(FWE) > 0.05), or working memory performance (P = 0.13, BF10 = 0.05) following real or sham cTBS. Our findings add to a growing body of literature suggesting the effects of cTBS are highly variable between individuals and question the notion that cTBS is a universal ‘inhibitory’ paradigm

Importance of Staff Training in Vip Juicemaker Oy

Human Resource Management (HRM) plays a significant role in the progress and development of any company or organization. Organizations apply modern techniques and strategies for effective management of the employees. This in turn improves the performance of the employees so that the organization can prosper. For this purpose companies try to develop new and unique techniques and strategies, which are beneficial for the employees and the company as a whole. One such strategy is training. It is considered to be an important strategy as it helps increase the efficiency of the employees and the productivity of the company. From the company’s perspective, training can be regarded as an investment which helps improve the employees’ attitude towards their work both on the professional and personal level and can assist in the smooth operation of the company. The objective of this research was to highlight the importance of training in organizations via a study conducted at VIP Juicemaker, a leading juice producer in Finland. The main purpose of the study was to understand the system of human resource management and the process of training in the case company. Furthermore, the study aimed to analyze the effect of training on the job satisfaction of the employees. Another objective of the study was to provide suggestions on how to improve the management system of the company and its training methods. In total ten interviews were hold among managers and staff. Questions were asked regarding the present HRM system and training facilities as well as processes in the company. The results are supported by theoretical studies of different of books, web books, web publications, internet articles, websites and reports on human resource management. The study concludes that HRM strategy is indeed very important for a company. The research results in the following suggestions: to hire a proficient human resource manager, to change the size of the company and to focus on the future of the company. It was also found out that the most of the workers are satisfied with their work and provision. However they still lack motivation and inspiration in performing for the development of the organization. Furthermore, the company is in progress to develop their new strategy and management system to achieve Big Hairy Audacious Goal

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

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 frst 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

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

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.Cross-sectional.University laboratory.Ten individuals with chronic LBP and 10 pain-free controls.Participants received four interventions in random order across separate sessions: 1) anodal tDCS to M1 + PES to the back muscles; 2)\ua0tDCS + 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.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.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

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

Abstract 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

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