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author:("Lewis, gyn")
1.  Quadriceps arthrogenic muscle inhibition: the effects of experimental knee joint effusion on motor cortex excitability 
Marked weakness of the quadriceps muscles is typically observed following injury, surgery or pathology affecting the knee joint. This is partly due to ongoing neural inhibition that prevents the central nervous system from fully activating the quadriceps, a process known as arthrogenic muscle inhibition (AMI). This study aimed to further investigate the mechanisms underlying AMI by exploring the effects of experimental knee joint effusion on quadriceps corticomotor and intracortical excitability.
Seventeen healthy volunteers participated in this study. Transcranial magnetic stimulation was used to measure quadriceps motor evoked potential area, short-interval intracortical inhibition, intracortical facilitation and cortical silent period duration before and after experimental knee joint effusion. Joint effusion was induced by the intraarticular infusion of dextrose saline into the knee.
There was a significant increase in quadriceps motor evoked potential area following joint infusion, both at rest (P = 0.01) and during voluntary muscle contraction (P = 0.02). Cortical silent period duration was significantly reduced following joint infusion (P = 0.02). There were no changes in short interval intracortical inhibition or intracortical facilitation over time (all P > 0.05).
The results of this study provide no evidence for a supraspinal contribution to quadriceps AMI. Paradoxically, but consistent with previous observations in patients with chronic knee joint pathology, quadriceps corticomotor excitability increased after experimental knee joint effusion. The increase in quadriceps corticomotor excitability may be at least partly mediated by a decrease in gamma-aminobutyric acid (GABA)-ergic inhibition within the motor cortex.
PMCID: PMC4271337  PMID: 25497133
2.  Influence of stimulation location and posture on the reliability and comfort of the nociceptive flexion reflex 
The lower limb nociceptive flexion reflex (NFR) is commonly used to assess the function of the nociceptive system. Currently, there is a lack of standardized stimulation procedures to determine the NFR threshold, making comparisons of thresholds across studies difficult.
To assess and compare the within- and between-session reliability of NFR threshold when elicited from two common stimulation locations: the medial arch of the foot (while standing) and the sural nerve (while seated).
A staircase procedure was used to determine NFR threshold in 20 healthy participants twice within one session and once more in a separate session approximately four days later. At both sessions, NFR threshold was determined from both medial arch and sural nerve stimulation. Comparisons of NFR threshold, reliability and participant discomfort ratings were made between the two stimulation locations.
NFR thresholds were statistically equivalent at the two stimulation locations, but there were more nonresponders and ratings of participant discomfort were significantly higher during stimulation over the sural nerve. Within-session reliability measures were superior for stimulation over the sural nerve; however, between-session measures were more reliable using stimulation over the medial arch of the foot.
The authors recommend stimulation over the medial arch of the foot while standing as the preferred location for eliciting the lower limb NFR, particularly if measurements are to be compared across multiple sessions.
PMCID: PMC3393053  PMID: 22518374
Flexion reflex; Lower limb; Reliability
3.  Reliability of the conditioned pain modulation paradigm to assess endogenous inhibitory pain pathways 
Conditioned pain modulation paradigms are often used to assess the diffuse noxious inhibitory control (DNIC) system. DNICs provide one of the main supraspinal pain inhibitory pathways and are impaired in several chronic pain populations. Only one previous study has examined the psychometric properties of the conditioned pain modulation technique and this study did not evaluate intersession reliability.
To evaluate and compare the intra- and intersession reliability of two conditioned pain modulation paradigms using different conditioning stimuli, and to determine the time course of conditioned pain inhibition following stimulus removal.
An electronic pressure transducer was used to determine the pressure-pain threshold at the knee during painful conditioning of the opposite hand using the ischemic arm test and the cold pressor test. Assessments were completed twice on one day and repeated once approximately three days later.
The two conditioning stimuli resulted in a similar increase in the pressure-pain threshold at the knee, reflecting presumed activation of the DNIC system. Intrasession intraclass correlation coefficients for the cold pressor (0.85) and ischemic arm tests (0.75) were excellent. The intersession intraclass correlation coefficient for the cold pressor test was good (0.66) but was poor for the ischemic arm test (−0.4). Inhibition of the pressure-pain threshold remained significant at 10 min following conditioning, but returned to baseline by 15 min.
Within-session reliability of DNIC assessment using conditioned pain modulation paradigms was excellent, but the applicability of assessing pain modulation over multiple sessions was influenced by the conditioning stimulus. The cold pressor test was the superior technique.
PMCID: PMC3393056  PMID: 22518372
Diffuse noxious inhibitory control; Pain; Reliability
Levels of evidence allow clinicians to appreciate the quality of a particular research paper quickly. The levels are generally set out in a hierarchical order, which is based largely upon the experimental design. While there are ideal designs for studies examining the effects of interventions, risk factors for a clinical condition or diagnostic testing, in most instances researchers have had to make compromises and these subsequently decrease the quality of their work. This paper provides information concerning how those compromises relate to subsequent levels that are given to a piece of research. It also provides an understanding of issues related to evaluating papers, and suggest ways in which the reader might discern how relevant a paper might be to one's clinical practice.
PMCID: PMC3474306  PMID: 23091779
levels of evidence; research design; study quality
5.  Mechanisms of quadriceps muscle weakness in knee joint osteoarthritis: the effects of prolonged vibration on torque and muscle activation in osteoarthritic and healthy control subjects 
Arthritis Research & Therapy  2011;13(5):R151.
A consequence of knee joint osteoarthritis (OA) is an inability to fully activate the quadriceps muscles, a problem termed arthrogenic muscle inhibition (AMI). AMI leads to marked quadriceps weakness that impairs physical function and may hasten disease progression. The purpose of the present study was to determine whether γ-loop dysfunction contributes to AMI in people with knee joint OA.
Fifteen subjects with knee joint OA and 15 controls with no history of knee joint pathology participated in this study. Quadriceps and hamstrings peak isometric torque (Nm) and electromyography (EMG) amplitude were collected before and after 20 minutes of 50 Hz vibration applied to the infrapatellar tendon. Between-group differences in pre-vibration torque were analysed using a one-way analysis of covariance, with age, gender and body mass (kg) as the covariates. If the γ-loop is intact, vibration should decrease torque and EMG levels in the target muscle; if dysfunctional, then torque and EMG levels should not change following vibration. One-sample t tests were thus undertaken to analyse whether percentage changes in torque and EMG differed from zero after vibration in each group. In addition, analyses of covariance were utilised to analyse between-group differences in the percentage changes in torque and EMG following vibration.
Pre-vibration quadriceps torque was significantly lower in the OA group compared with the control group (P = 0.005). Following tendon vibration, quadriceps torque (P < 0.001) and EMG amplitude (P ≤0.001) decreased significantly in the control group but did not change in the OA group (all P > 0.299). Hamstrings torque and EMG amplitude were unchanged in both groups (all P > 0.204). The vibration-induced changes in quadriceps torque and EMG were significantly different between the OA and control groups (all P < 0.011). No between-group differences were observed for the change in hamstrings torque or EMG (all P > 0.554).
γ-loop dysfunction may contribute to AMI in individuals with knee joint OA, partially explaining the marked quadriceps weakness and atrophy that is often observed in this population.
PMCID: PMC3308081  PMID: 21933392
6.  Co-contraction modifies the stretch reflex elicited in muscles shortened by a joint perturbation 
Simultaneous contraction of agonist and antagonist muscles acting about a joint influences joint stiffness and stability. Although several studies have shown that reflexes in the muscle lengthened by a joint perturbation are modulated during co-contraction, little attention has been given to reflex regulation in the antagonist (shortened) muscle. The goal of the present study was to determine whether co-contraction gives rise to altered reflex regulation across the joint by examining reflexes in the muscle shortened by a joint perturbation. Reflexes were recorded from electromyographic activity in elbow flexors and extensors while positional perturbations to the elbow joint were applied. Perturbations were delivered during isolated activation of the flexor or extensor muscles as well as during flexor and extensor co-contraction. Across the group, the shortening reflex in the elbow extensor switched from suppression during isolated extensor muscle activation to facilitation during co-contraction. The shortening reflex in the elbow flexor remained suppressive during co-contraction but was significantly smaller compared to the response obtained during isolated elbow flexor activation. This response in the shortened muscle was graded by the level of activation in the lengthened muscle. The lengthening reflex did not change during co-contraction. These results support the idea that reflexes are regulated across multiple muscles around a joint. We speculate that the facilitatory response in the shortened muscle arises through a fast-conducting oligosynaptic pathway involving Ib interneurons.
PMCID: PMC3045052  PMID: 20878148
Stretch reflex; Co-contraction; Upper limb; Shortening reaction
7.  Interactions With Compliant Loads Alter Stretch Reflex Gains But Not Intermuscular Coordination 
Journal of neurophysiology  2008;99(5):2101-2113.
The human motor system regulates arm mechanics to produce stable postures during interactions with different physical environments. This occurs partly via involuntary mechanisms, including stretch reflexes. Previous single-joint studies demonstrated enhanced reflex sensitivity during interactions with compliant environments, suggesting reflex gain increases to enhance limb stability when that stability is not provided by the environment. This study examined whether similar changes in reflex gain are present throughout the limb following perturbations that simultaneously influence multiple joints. Furthermore, we investigated whether any observed modulation was accompanied by task-specific changes in reflex coordination across muscles, a question that cannot be addressed using single-joint perturbations. Reflexes were elicited during the maintenance of posture by perturbing the arm with a three degrees of freedom robot, configured to have isotropic stiffness of either 10 N/m (compliant) or 10 kN/m (stiff). Perturbation characteristics were matched in both environments. Reflex magnitude was quantified by the average rectified electromyogram, recorded from eight muscles crossing the elbow and shoulder. Reflex coordination was assessed using independent components analysis to compare reflex activation patterns during interactions with stiff and compliant environments. Stretch reflex sensitivity increased significantly in all muscles during interactions with the compliant environment and these changes were not due to changes in background muscle activity. However, there was no significant difference in the reflex coordination patterns observed during interactions with the stiff and compliant environments. These results suggest that reflex modulation occurred through altered use of fixed muscle coordination patterns rather than through a change in reflex coordination.
PMCID: PMC2810681  PMID: 18287550
8.  The effect of task instruction on the excitability of spinal and supraspinal reflex pathways projecting to the biceps muscle 
There is controversy within the literature regarding the influence of task instruction on the size of the long-latency stretch reflex (M2) elicited by a joint displacement. The aim of this study was to investigate if the previously reported task-dependent modulation of the M2 is specific to the M2 or can be explained by an early release of the intended voluntary response. We took advantage of the fact that the M2 is absent when the duration of the applied perturbation is less than a critical time period. This allowed us to examine modulation of muscle activity with and without the contribution of the M2. In addition, we applied transcranial magnetic stimulation (TMS) over the primary motor cortex to examine the modulation of corticomotor excitability with task instruction. Elbow joint extension displacements were used to elicit a stretch reflex in the biceps muscle. Subjects were instructed to “do not intervene” (DNI) with the applied perturbation, or to oppose the perturbation by activating the elbow flexors in response to the perturbation (FLEX). Electromyographic (EMG) activity in the time period corresponding to the M2 was significantly facilitated in the FLEX task instruction both with and without the presence of the M2. Motor evoked potentials (MEPs) elicited by TMS were also facilitated during the FLEX condition in the absence of the M2. EMG and MEP responses were not facilitated until immediately prior to the onset of the M2. Paired-pulse TMS revealed a significant reduction in short-interval intracortical inhibition (SICI) during the M2 response, but the level of SICI was not altered by the task instruction. We conclude that the task-dependent modulation of the biceps M2 results, at least in part, from an early release of the prepared movement and is accompanied by an increase in corticospinal excitability that is not specific to the M2 pathway. Task-dependent modulation of the response cannot be explained by an alteration in the excitability of intracortical inhibitory circuits.
PMCID: PMC2756617  PMID: 16676166
Stretch reflex; Upper limb; Transcranial magnetic stimulation; Voluntary movement
9.  Side of lesion influences interhemispheric inhibition in subjects with post-stroke hemiparesis 
To examine changes in interhemispheric inhibition (IHI) during homologous muscle activation in healthy subjects and in people with hemiparesis.
IHI in the abductor pollicus brevis (APB) muscle was examined using paired transcranial magnetic stimulation. Stimuli were delivered while the target APB was at rest or activated, and while the non-target contralateral APB was at rest or activated.
In control subjects, IHI in the resting target APB was enhanced during activation of the contralateral APB, and was greater from the dominant hemisphere to the non-dominant. In stroke subjects, IHI in the non-affected APB was not modulated during voluntary activation of the affected APB, but was influenced by the prior dominance of affected hemisphere. Bilateral muscle activation did not elicit any changes in IHI in either group.
IHI is asymmetrical between hemispheres but only when the target muscle is at rest. Subjects with stroke have an impaired ability to modulate IHI during unilateral muscle activation.
In people with stroke, the extent and modulation of interhemispheric transfer is influenced by the prior dominance of the affected hemisphere. This may impact on the efficacy of treatment interventions incorporating bilateral activation.
PMCID: PMC2200632  PMID: 17967558
hemiparesis; interhemispheric inhibition; transcranial magnetic stimulation; bilateral muscle activation

Results 1-9 (9)