A computational study of how an α- to γ-motoneurone collateral can mitigate velocity-dependent stretch reflexes during voluntary movement.

The primary motor cortex does not uniquely or directly produce alpha motoneurone (α-MN) drive to muscles during voluntary movement. Rather, α-MN drive emerges from the synthesis and competition among excitatory and inhibitory inputs from multiple descending tracts, spinal interneurons, sensory inputs, and proprioceptive afferents. One such fundamental input is velocity-dependent stretch reflexes in lengthening muscles, which should be inhibited to enable voluntary movement. It remains an open question, however, the extent to which unmodulated stretch reflexes disrupt voluntary movement, and whether and how they are inhibited in limbs with numerous multiarticular muscles. We used a computational model of a Rhesus Macaque arm to simulate movements with feedforward α-MN commands only, and with added velocity-dependent stretch reflex feedback. We found that velocity-dependent stretch reflex caused movement-specific, typically large and variable disruptions to arm movements. These disruptions were greatly reduced when modulating velocity-dependent stretch reflex feedback (i) as per the commonly proposed (but yet to be clarified) idealized alpha-gamma (α-γ) coactivation or (ii) an alternative α-MN collateral projection to homonymous γ-MNs. We conclude that such α-MN collaterals are a physiologically tenable propriospinal circuit in the mammalian fusimotor system. These collaterals could still collaborate with α-γ coactivation, and the few skeletofusimotor fibers (ß-MNs) in mammals, to create a flexible fusimotor ecosystem to enable voluntary movement. By locally and automatically regulating the highly nonlinear neuro-musculo-skeletal mechanics of the limb, these collaterals could be a critical low-level enabler of learning, adaptation, and performance via higher-level brainstem, cerebellar, and cortical mechanisms.

Tonic stretch reflex threshold as a measure of disordered motor control and spasticity - A critical review.

The Tonic Stretch Reflex Threshold (TSRT) is the joint angle or muscle length (λ) at which muscle activation begins. In spasticity, the TSRT abnormally lies inside the biomechanical joint range. It is determined by measuring the Dynamic Stretch Reflex Thresholds (DSRTs) by stretching the resting muscle at different velocities. The metric µ, characterizes the velocity-sensitivity of the DSRTs and is expressed as the time required to lengthen the passive muscles from DSRT to TSRT at the respective stretch velocity. The original formulation of the TSRT, DSRT and µ is summarized. Then, a thorough search of literature prior to December 2023 was conducted that returned 25 papers that have used the technique. Eleven of these papers come from the research group of the authors, including 1 reporting on treatment effects. Of the remaining 14 papers, 11 report variations of the methodology with different populations and 3 report on the effects of an intervention. The review discusses how specific modifications to data collection and analysis procedures have either improved the methodology or, in some cases, led to uninterpretable results. The influence of modifications to the data collection and analysis procedures is discussed.

Inverting a model of neuromuscular control to estimate descending activation patterns that generate fast-reaching movements.

Reaching movements generally show smooth kinematic profiles that are invariant across varying movement speeds even as interaction torques and muscle properties vary nonlinearly with speed. How the brain brings about these invariant profiles is an open question. We developed an analytical inverse dynamics method to estimate descending activation patterns directly from observed joint angle trajectories based on a simple model of the stretch reflex, and of muscle and biomechanical dynamics. We estimated descending activation patterns for experimental data from eight different planar two-joint movements performed at two movement times (fast: 400 ms; slow: 800 ms). The temporal structure of descending activation differed qualitatively across speeds, consistent with the idea that the nervous system uses an internal model to generate anticipatory torques during fast movement. This temporal structure also depended on the cocontraction level of antagonistic muscle groups. Comparing estimated muscle activation and descending activation revealed the contribution of the stretch reflex to movement generation that was found to set in after about 20% of movement time.NEW & NOTEWORTHY By estimating descending activation patterns directly from observed movement kinematics based on a model of the dynamics of the stretch reflex, of muscle force generation, and of the biomechanics of the limb, we observed how brain signals must be temporally structured to enable fast movement.

Implementation of surface mechanomyography as a novel approach for objective evaluation of phasic muscle stretch reflexes in people with type 2 diabetes.

INTRODUCTION: Diabetic peripheral neuropathy is the most common complication of diabetes producing metabolic disruptions in the peripheral nervous system. Alteration in the predictable nature of tendon reflexes is the most common indicator suggesting the possibility of diabetic neuropathy. Evaluation of tendon reflexes is a part of various clinical scoring systems that assess neuropathy. The conventional reflex grading scales are subjective, lack temporal data, and have high inter-rater variability. Hence, an indigenous quantification tool was developed to evaluate the tendon reflexes in order to assess diabetic peripheral neuropathy. MATERIALS AND METHODS: A cross-sectional study was carried out in 140 healthy volunteers and 140 patients with type 2 diabetes. The mean age of controls and diabetics (49.1 ± 8.9, 50.7 ± 7.5) years, weight (66.9 ± 9.4, 69.8 ± 11.5) kilograms and BMI (24.5 ± 3.8, 26.1 ± 4.7), respectively. All of them are subjected to evaluation of tendon reflexes using the reflex quantification tool comprised of surface mechanomyography and electrogoniometry that can provide various static and dynamic variables of tendon reflex. RESULTS: The dynamic variables such as reflex amplitude, muscle velocity and angular velocity were significantly low in diabetic patients (p: <0.001) whereas latency and duration (p: <0.001) were prolonged. Furthermore, no significant difference was observed in the application of tendon striking force (p: 0.934) among the participants. CONCLUSION: The current study demonstrates that the proposed reflex quantification tool provides several dynamic variables of patellar tendon reflex, which are significantly affected and altered in diabetic patients suggesting the involvement of peripheral neurons.

Upper motor neuron assessment in amyotrophic lateral sclerosis using the patellar tendon reflex and motor-evoked potentials to the lower limbs.

Amyotrophic lateral sclerosis (ALS) diagnosis relies on signs of progressive damage to both lower motoneuron (LMN), given by clinical examination and electromyography (EMG), and upper motoneuron (UMN), given by clinical examination only. Recognition of UMN involvement, however, is still difficult, so that diagnostic delay often remains too long. Shortening the time to clinical and genetic diagnosis is essential in order to provide accurate information to patients and families, avoid time-consuming investigations and for appropriate care management. This study investigates whether combined patellar tendon reflex recording with motor-evoked potentials to the lower limbs (T-MEP-LL) is relevant to assess corticospinal function in ALS, so that it might serve as a tool improving diagnosis. T-MEP-LL were recorded in 135 patients with suspected motor neuron disease (MND) from February 2010 to March 2021. The sensitivity, specificity, and ability to improve diagnosis when added to Awaji and Gold Coast criteria were determined. The main finding of the study is that T-MEP-LL can detect UMN dysfunction with a 70% sensitivity and 63% specificity when UMN clinical signs are lacking. The sensitivity reaches 82% when considering all MND patients. Moreover, at first evaluation, using T-MEP-LL to quantify reflex briskness and to measure central conduction time, can improve the diagnostic accuracy. T-MEP-LL is easy to perform and does not need any electrical stimulation, making the test rapid, and painless. By the simultaneous quantification of both UMN and LMN system, it could also help to identify different phenotype with more accuracy than clinical examination in this broad-spectrum pathology. The question whether T-MEP-LL could further be a real biomarker need further prospective studies.

A single sequence of intermittent hypoxia does not alter stretch reflex excitability in able-bodied individuals.

Spasticity attributable to exaggerated stretch reflex pathways, particularly affecting the ankle plantar flexors, often impairs overground walking in persons with incomplete spinal cord injury. Compelling evidence from rodent models underscores how exposure to acute intermittent hypoxia (AIH) can provide a unique medium to induce spinal plasticity in key inhibitory pathways mediating stretch reflex excitability and potentially affect spasticity. In this study, we quantify the effects of a single exposure to AIH on the stretch reflex in able-bodied individuals. We hypothesized that a single sequence of AIH will increase the stretch reflex excitability of the soleus muscle during ramp-and-hold angular perturbations applied to the ankle joint while participants perform passive and volitionally matched contractions. Our results revealed that a single AIH exposure did not significantly change the stretch reflex excitability during both passive and active matching conditions. Furthermore, we found that able-bodied individuals increased their stretch reflex response from passive to active matching conditions after both sham and AIH exposures. Together, these findings suggest that a single AIH exposure might not engage inhibitory pathways sufficiently to alter stretch reflex responses in able-bodied persons. However, the generalizability of our present findings requires further examination during repetitive exposures to AIH along with potential reflex modulation during functional movements, such as overground walking.

Tactile stimulation restores inhibited stretch reflex attributable to attenuation of Ia afferents during surprise landing.

Arthrogenic muscle inhibition (AMI) is induced by pathological knee conditions. The present study aimed to investigate the effect of tactile stimulation on reflex changes induced by simulated AMI during unpredictable landing performances. Twenty participants performed six unilateral landing tasks: 15 cm normal landing (15NL), 30 cm normal landing (30NL), surprise landing (SL), 30 cm normal landing following vibration (30NLV), SL following vibration (SLV), and SL following vibration with Kinesiology tape (SLK). For SL, the solid landing platform (15 cm) was removed and replaced by a false floor. Since the false floor dislodged easily under load, participants unpredictably fell through the platform to the actual landing surface 15 cm below. After completing 15NL, 30NL, and SL, vibration was applied to participants' knees to induce neurological changes similar to AMI. After vibration, participants performed 30NLV, SLV, and SLK in a random order. EMG signals in the post-landing short latency (31-60 ms) and medium latency (61-90 ms) periods were examined. EMG signals from the vastus lateralis (VL), vastus medialis (VM), and biceps femoris (BF) were recorded and compared between tasks. EMG signals of all muscles in SL were significantly enhanced in the medium latency period as compared with 30NL. Enhanced EMG signals in SL were suppressed by vibration stimulation in the VL, but the suppressed EMG signals were restored after cutaneous stimulation with Kinesiology tape (p < 0.01). Our findings suggest that AMI could alter motor control patterns during unpredictable landing and that tactile stimulation could restore the altered motor control to a normal state.

Sensorimotor control in the congenital absence of functional muscle spindles.

Hereditary sensory and autonomic neuropathy type III (HSAN III), also known as familial dysautonomia or Riley-Day syndrome, results from an autosomal recessive genetic mutation that causes a selective loss of specific sensory neurones, leading to greatly elevated pain and temperature thresholds, poor proprioception, marked ataxia and disturbances in blood pressure control. Stretch reflexes are absent throughout the body, which can be explained by the absence of functional muscle spindle afferents - assessed by intraneural microelectrodes inserted into peripheral nerves in the upper and lower limbs. This also explains the greatly compromised proprioception at the knee joint, as assessed by passive joint-angle matching. Moreover, there is a tight correlation between loss of proprioceptive acuity at the knee and the severity of gait impairment. Surprisingly, proprioception is normal at the elbow, suggesting that participants are relying more on sensory cues from the overlying skin; microelectrode recordings have shown that myelinated tactile afferents in the upper and lower limbs appear to be normal. Nevertheless, the lack of muscle spindles does affect sensorimotor control in the upper limb: in addition to poor performance in the finger-to-nose test, manual performance in the Purdue pegboard task is much worse than in age-matched healthy controls. Unlike those rare individuals with large-fibre sensory neuropathy, in which both muscle spindle and cutaneous afferents are absent, those with HSAN III present as a means of assessing sensorimotor control following the selective loss of muscle spindle afferents.

Differentiation in additive and multiplicative inputs to motoneuron pool as origins of spasticity - a neuromorphic modeling study.

Spasticity is characterized by a velocity-dependent increase in the tonic stretch reflex. Evidence suggests that spasticity originates from hyperactivity in the descending tract or reflex loop. To pinpoint the source of hyperactivity, however, is difficult due to lack of human data in-vivo. Thus, we implemented a neuromorphic model to revive the neurodynamics with spiking neuronal activity. Two types of input were modeled: (1) the additive condition (ADD) to apply tonic synaptic inputs directly into the reflex loop; (2) the multiplicative (MUL) condition to adjust the loop gains within the reflex loop. Results show that both conditions produced antagonist EMG responses resembling patient data. The timing of spasticity is more sensitive to the ADD condition, whereas the amplitude of spastic EMG is more sensitive to the MUL condition. In conclusion, our model shows that both additive and multiplicative hyperactivities suffice to elicit velocity-dependent spastic electromyographic signals (EMG), but with different sensitivities. This simulation study suggests that spasticity caused by different origins may be discernable by the progression of severity, which may help individualized goalsetting and parameter-selection in rehabilitation.Clinical Relevance-Potential application of neuromorphic modeling on spasticity includes selection of parameters for therapeutic plans, such as movement range, repetition, and load.

Evaluation of stretch reflex synergies in the upper limb using principal component analysis (PCA).

The dynamic nature of movement and muscle activation emphasizes the importance of a sound experimental design. To ensure that an experiment determines what we intend, the design must be carefully evaluated. Before analyzing data, it is imperative to limit the number of outliers, biases, and skewness. In the present study, a simple center-out experiment was performed by 16 healthy volunteers. The experiment included three load conditions, two preparatory delays, two perturbations, and four targets placed along a diagonal path on a 2D plane. While the participants performed the tasks, the activity of seven arm muscles were monitored using surface electromyography (EMG). Principal component analysis (PCA) was used to evaluate the study design, identify muscle synergies, and assess the effects of individual quirks. With PCA, we can identify the trials that trigger stretch reflexes and pinpoint muscle synergies. The posterior deltoid, triceps long head, and brachioradialis were engaged when targets were in the direction of muscle shortening and the perturbation was applied in the opposite direction. Similarly, the pectoralis and anterior deltoid were engaged when the targets were in the direction of muscle shortening and the perturbation was applied in the opposite direction. The stretch reflexes were not triggered when the perturbation brought the hand in the direction of, or into the target, except if the muscle was pre-loaded. The use of PCA was also proven valuable when evaluating participant performance. While individual quirks are to be expected, failure to perform trials as expected can adversely affect the study results.

Goal-directed modulation of stretch reflex gains is reduced in the non-dominant upper limb.

Most individuals experience their dominant arm as being more dexterous than the non-dominant arm, but the neural mechanisms underlying this asymmetry in motor behaviour are unclear. Using a delayed-reach task, we have recently demonstrated strong goal-directed tuning of stretch reflex gains in the dominant upper limb of human participants. Here, we used an equivalent experimental paradigm to address the neural mechanisms that underlie the preparation for reaching movements with the non-dominant upper limb. There were consistent effects of load, preparatory delay duration and target direction on the long latency stretch reflex. However, by comparing stretch reflex responses in the non-dominant arm with those previously documented in the dominant arm, we demonstrate that goal-directed tuning of short and long latency stretch reflexes is markedly weaker in the non-dominant limb. The results indicate that the motor performance asymmetries across the two upper limbs are partly due to the more sophisticated control of reflexive stiffness in the dominant limb, likely facilitated by the superior goal-directed control of muscle spindle receptors. Our findings therefore suggest that fusimotor control may play a role in determining performance of complex motor behaviours and support existing proposals that the dominant arm is better supplied than the non-dominant arm for executing more complex tasks, such as trajectory control.

Muscular reflex gains reflect changes of mind in reaching.

Decisions for action are accompanied by a continual processing of sensory information, sometimes resulting in a revision of the initial choice, called a change of mind (CoM). Although the motor system is tuned during the formation of a reach decision, it is unclear whether its preparatory state differs between CoM and non-CoM decisions. To test this, participants (n = 14) viewed a random-dot motion (RDM) stimulus of various coherence levels for a random viewing duration. At the onset of a mechanical perturbation that rapidly stretched the pectoralis muscle, they indicated the perceived motion direction by making a reaching movement to one of two targets. Using electromyography (EMG), we quantified the reflex gains of the pectoralis and posterior deltoid muscles. Results show that reflex gains scaled with both the coherence level and the viewing duration of the stimulus. We fit a drift diffusion model (DDM) to the behavioral choices. The decision variable (DV), derived from the DDM, correlated well with the measured reflex gain at the single-trial level. However, when matched on DV magnitude, reflex gains were significantly lower in CoM than non-CoM trials. We conclude that the internal state of the motor system, as measured by the spinal reflexes, reflects the continual deliberation on sensory evidence for action selection, including the postdecisional evidence that can lead to a change of mind.NEW & NOTEWORTHY Using behavioral findings, EMG, and computational modeling, we show that not only the perceptual decision outcome but also the accumulating evidence for that outcome is continuously sent to the relevant muscles. Moreover, we show that an upcoming change of mind can be detected in the motor periphery, suggesting that a correlate of the internal decision making process is being sent along.

A Method for Quantification of Stretch Reflex Excitability During Ballistic Reaching.

Stretch reflexes are crucial for performing accurate movements and providing rapid corrections for unpredictable perturbations. Stretch reflexes are modulated by supraspinal structures via corticofugal pathways. Neural activity in these structures is difficult to observe directly, but the characterization of reflex excitability during volitional movement can be used to study how these structures modulate reflexes and how neurological injuries impact this control, such as in spasticity after stroke. We have developed a novel protocol to quantify stretch reflex excitability during ballistic reaching. This novel method was implemented using a custom haptic device (NACT-3D) capable of applying high-velocity (270 °/s) joint perturbations in the plane of the arm while participants performed 3D reaching tasks in a large workspace. We assessed the protocol on four participants with chronic hemiparetic stroke and two control participants. Participants reached ballistically from a near to a far target, with elbow extension perturbations applied in random catch trials. Perturbations were applied before movement, during the early phase of movement, or near peak movement velocity. Preliminary results show that stretch reflexes were elicited in the stroke group in the biceps muscle during reaching, as measured by electromyographic (EMG) activity both before (pre-motion phase) and during (early motion phase) movement. Reflexive EMG was also seen in the anterior deltoid and pectoralis major in the pre-motion phase. In the control group, no reflexive EMG was seen, as expected. This newly developed methodology allows the study of stretch reflex modulation in new ways by combining multijoint movements with haptic environments and high-velocity perturbations.

Rigidity in Parkinson's disease: evidence from biomechanical and neurophysiological measures.

Although rigidity is a cardinal motor sign in patients with Parkinson's disease (PD), the instrumental measurement of this clinical phenomenon is largely lacking, and its pathophysiological underpinning remains still unclear. Further advances in the field would require innovative methodological approaches able to measure parkinsonian rigidity objectively, discriminate the different biomechanical sources of muscle tone (neural or visco-elastic components), and finally clarify the contribution to 'objective rigidity' exerted by neurophysiological responses, which have previously been associated with this clinical sign (i.e. the long-latency stretch-induced reflex). Twenty patients with PD (67.3 ± 6.9 years) and 25 age- and sex-matched controls (66.9 ± 7.4 years) were recruited. Rigidity was measured clinically and through a robotic device. Participants underwent robot-assisted wrist extensions at seven different angular velocities randomly applied, when ON therapy. For each value of angular velocity, several biomechanical (i.e. elastic, viscous and neural components) and neurophysiological measures (i.e. short and long-latency reflex and shortening reaction) were synchronously assessed and correlated with the clinical score of rigidity (i.e. Unified Parkinson's Disease Rating Scale-part III, subitems for the upper limb). The biomechanical investigation allowed us to measure 'objective rigidity' in PD and estimate the neuronal source of this phenomenon. In patients, 'objective rigidity' progressively increased along with the rise of angular velocities during robot-assisted wrist extensions. The neurophysiological examination disclosed increased long-latency reflexes, but not short-latency reflexes nor shortening reaction, in PD compared with control subjects. Long-latency reflexes progressively increased according to angular velocities only in patients with PD. Lastly, specific biomechanical and neurophysiological abnormalities correlated with the clinical score of rigidity. 'Objective rigidity' in PD correlates with velocity-dependent abnormal neuronal activity. The observations overall (i.e. the velocity-dependent feature of biomechanical and neurophysiological measures of objective rigidity) would point to a putative subcortical network responsible for 'objective rigidity' in PD, which requires further investigation.

Assessing shoulder muscle stretch reflexes following breast cancer treatment and postmastectomy breast reconstruction.

Muscle stiffness is altered following postmastectomy breast reconstruction and breast cancer treatment. The exact mechanisms underlying these alterations are unknown; however, muscle stretch reflexes may play a role. This work examined short- (SLR) and long-latency (LLR) shoulder muscle stretch reflexes in breast cancer survivors. Forty-nine patients who had undergone postmastectomy breast reconstruction, 17 who had undergone chemoradiation, and 18 healthy, age-matched controls were enrolled. Muscle activity was recorded from the clavicular and sternocostal regions of the pectoralis major and anterior, middle, and posterior deltoids during vertical ab/adduction or horizontal flex/extension perturbations while participants maintained minimal torques. SLR and LLR were quantified for each muscle. Our major finding was that following postmastectomy breast reconstruction, SLR and LLR are impaired in the clavicular region of the pectoralis major. Individuals who had chemoradiation had impaired stretch reflexes in the clavicular and sternocostal region of the pectoralis major, anterior, middle, and posterior deltoid. These findings indicate that breast cancer treatments alter the regulation of shoulder muscle stretch reflexes and may be associated with surgical or nonsurgical damage to the pectoral fascia, muscle spindles, and/or sensory Ia afferents.NEW & NOTEWORTHY Shoulder muscle stretch reflexes may be impacted following postmastectomy breast reconstruction and chemoradiation. Here, we examined short- and long-latency shoulder muscle stretch reflexes in two experiments following common breast reconstruction procedures and chemoradiation. We show impairments in pectoralis major stretch reflexes following postmastectomy breast reconstruction and pectoralis major and deltoid muscle stretch reflexes following chemoradiation. These findings indicate that breast cancer treatments alter the regulation of shoulder muscle stretch reflexes.

Assistive Loading Promotes Goal-Directed Tuning of Stretch Reflex Gains.

Voluntary movements are prepared before they are executed. Preparatory activity has been observed across the CNS and recently documented in first-order neurons of the human PNS (i.e., in muscle spindles). Changes seen in sensory organs suggest that independent modulation of stretch reflex gains may represent an important component of movement preparation. The aim of the current study was to further investigate the preparatory modulation of short-latency stretch reflex responses (SLRs) and long-latency stretch reflex responses (LLRs) of the dominant upper limb of human subjects. Specifically, we investigated how different target parameters (target distance and direction) affect the preparatory tuning of stretch reflex gains in the context of goal-directed reaching, and whether any such tuning depends on preparation duration and the direction of background loads. We found that target distance produced only small variations in reflex gains. In contrast, both SLR and LLR gains were strongly modulated as a function of target direction, in a manner that facilitated the upcoming voluntary movement. This goal-directed tuning of SLR and LLR gains was present or enhanced when the preparatory delay was sufficiently long (>250 ms) and the homonymous muscle was unloaded [i.e., when a background load was first applied in the direction of homonymous muscle action (assistive loading)]. The results extend further support for a relatively slow-evolving process in reach preparation that functions to modulate reflexive muscle stiffness, likely via the independent control of fusimotor neurons. Such control can augment voluntary goal-directed movement and is triggered or enhanced when the homonymous muscle is unloaded.

Combined tendon reflex and motor evoked potential recordings in amyotrophic lateral sclerosis.

OBJECTIVE: This retrospective (case-control) collaborative study evaluates tendon reflex recordings combined with transcranial magnetic stimulation motor evoked potentials recordings (T-MEPs) at lower limbs in amyotrophic lateral sclerosis (ALS). METHODS: T-MEPs were recorded in 97 ALS patients distinguished according to their patellar reflex briskness. Patients' electrophysiological data were compared with values measured in 60 control patients matched for age and height. Correlations studies between parameters or with some patients' clinical characteristics were also performed. RESULTS: The central motor conduction time yields the highest sensitivity (82%) and specificity (93%), allowing twice more upper motor neuron (UMN) dysfunction detection than clinical examination, and being more altered in late stages of the disease. The T response to MEP response amplitude ratio (T/MEP ar) is nearly as sensitive to detect ALS and better identifies abnormal hyperreflexia. It is not correlated with evolutive stage, contrarily to conduction time-related parameters. In addition, T-MEPs detect asymmetries escaping clinical examination. CONCLUSIONS: The corticospinal conduction to lower limbs is slowed in ALS. The T/MEP ar helps deciding when patellar reflexes are abnormal in a given patient suspected of ALS. SIGNIFICANCE: The T-MEP technique provide powerful electrophysiological biomarkers of UMN involvement in ALS. This simple and painless procedure introduces the clinically useful concept of electrophysiological hyperreflexia and might be expanded to future exploration of proximal upper limbs and bulbar territories.

Short-latency stretch reflexes depend on the balance of activity in agonist and antagonist muscles during ballistic elbow movements.

The spinal stretch reflex is a fundamental building block of motor function, with a sensitivity that varies continuously during movement and when changing between movement and posture. Many have investigated task-dependent reflex sensitivity, but few have provided simple, quantitative analyses of the relationship between the volitional control and stretch reflex sensitivity throughout tasks that require coordinated activity of several muscles. Here, we develop such an analysis and use it to test the hypothesis that modulation of reflex sensitivity during movement can be explained by the balance of activity within agonist and antagonist muscles better than by activity only in the muscle homonymous with the reflex. Subjects completed hundreds of flexion and extension movements as small, pseudorandom perturbations of elbow angle were applied to obtain estimates of stretch reflex amplitude throughout the movement. A subset of subjects performed a postural control task with muscle activities matched to those during movement. We found that reflex modulation during movement can be described by background activity in antagonist muscles about the elbow much better than by activity only in the muscle homonymous to the reflex (P < 0.001). Agonist muscle activity enhanced reflex sensitivity, whereas antagonist activity suppressed it. Surprisingly, the magnitude of these effects was similar, suggesting a balance of control between agonists and antagonists very different from the dominance of sensitivity to homonymous activity during posture. This balance is due to a large decrease in sensitivity to homonymous muscle activity during movement rather than substantial changes in the influence of antagonistic muscle activity.NEW & NOTEWORTHY This study examined the sensitivity of the stretch reflexes elicited in elbow muscles to the background activity in these same muscles during movement and postural tasks. We found a heightened reciprocal control of reflex sensitivity during movement that was not present during maintenance of posture. These results help explain previous discrepancies in reflex sensitivity measured during movement and posture and provide a simple model for assessing their contributions to muscle activity in both tasks.

Surgical results for cervical spondylotic myelopathy with inconsistent between deep tendon reflex findings and magnetic resonance imaging findings.

BACKGROUND: To evaluate the surgical results of patients with cervical spondylotic myelopathy (CSM) with inconsistency between deep tendon reflex findings and cervical magnetic resonance imaging (MRI) findings and to analyze the differences between patients with good and poor surgical outcomes. METHODS: We evaluated 50 subjects with CSM (30 males, 20 females; mean age: 70.4 years) who underwent posterior surgery and were followed for at least 1 year postoperatively. Matched CSM was defined as a consistent preoperative neurological pattern determined by deep tendon reflex and cervical MRI T2-weighted high-signal intramedullary area or stenosis in the most cranial compression levels. A lack of consistency was classified as unmatched CSM. Recovery rate (RR) according to Japanese Orthopaedic Association (JOA) scoring preoperatively and at 1 year postoperatively were compared between the groups. RESULTS: The matched and unmatched CSM group included 27 subjects (13 males, 14 females; mean age: 68.2 years) and 23 subjects (17 males, 6 females; mean age: 72.8 years), respectively. RR was significantly higher in the matched CSM group (56.1 ± 3.7 % vs 36.8 ± 2.7 %; p = 0.002). Unmatched CSM was significantly associated with a lower RR independently of sex, patient age, surgical procedure, preoperative JOA score, diagnosis levels, and complication of diabetes. CONCLUSIONS: Postoperative JOA score RR was significantly diminished among unmatched CSM patients comprising of 46% of cases. Some patients with unmatched CSM had multiple levels of spinal canal stenosis, foraminal stenosis, and peripheral neuropathy, suggesting that surgical results were poorer than those of matched CSM.

A Velocity Stretch Reflex Threshold Based on Muscle-Tendon Unit Peak Acceleration to Detect Possible Occurrences of Spasticity during Gait in Children with Cerebral Palsy.

Spasticity might affect gait in children with cerebral palsy. Quantifying its occurrence during locomotion is challenging. One approach is to determine kinematic stretch reflex thresholds, usually on the velocity, during passive assessment and to search for their exceedance during gait. These thresholds are determined through EMG-Onset detection algorithms, which are variable in performance and sensitive to noisy data, and can therefore lack consistency. This study aimed to evaluate the feasibility of determining the velocity stretch reflex threshold from maximal musculotendon acceleration. Eighteen children with CP were recruited and underwent clinical gait analysis and a full instrumented assessment of their soleus, gastrocnemius lateralis, semitendinosus, and rectus femoris spasticity, with EMG, kinematics, and applied forces being measured simultaneously. Using a subject-scaled musculoskeletal model, the acceleration-based stretch reflex velocity thresholds were determined and compared to those based on EMG-Onset determination. Their consistencies according to physiological criteria, i.e., if the timing of the threshold was between the beginning of the stretch and the spastic catch, were evaluated. Finally, two parameters designed to evaluate the occurrence of spasticity during gait, i.e., the proportion of the gait trial time with a gait velocity above the velocity threshold and the number of times the threshold was exceeded, were compared. The proposed method produces velocity stretch reflex thresholds close to the EMG-based ones. For all muscles, no statistical difference was found between the two parameters designed to evaluate the occurrence of spasticity during gait. Contrarily to the EMG-based methods, the proposed method always provides physiologically consistent values, with median electromechanical delays of between 50 and 130 ms. For all subjects, the semitendinosus velocity during gait usually exceeded its stretch reflex threshold, while it was less frequent for the three other muscles. We conclude that a velocity stretch reflex threshold, based on musculotendon acceleration, is a reliable substitute for EMG-based ones.