Long-latency Reflex Research Articles

The intelligent reflex

ABSTRACTThe seeming distinction between motor and cognitive skills has hinged on the fact that the former are automatic and non-propositional (knowing-how), whereas the latter are slow and deliberative (knowing-that). Here, the physiological and behavioral phenomenon of long-latency stretch reflexes is used to show that “knowing-that” can be incorporated into “knowing-how,” either immediately or through learning. The experimental demonstration that slow computations can, with practice, be cached for fast retrieval, without the need for re-computation, dissolves the intellectualist/anti-intellectualist distinction: All complex human tasks, at any level of expertise, are a combination of intelligent reflexes and deliberative decisions.

Shoulder reflexes integrate elbow information at "long-latency" delay throughout a corrective action.

Previous studies have demonstrated a progression of function when healthy subjects counter a sudden mechanical load. Short-latency reflexes are linked to local stretch of the particular muscle and its antagonist. Long-latency reflexes integrate stretch information from both local sources and muscles crossing remote joints appropriate for a limb's mechanical interactions. Unresolved is how sensory information is processed throughout the corrective response, since capabilities at some time can be produced by circuits acting at that delay and at briefer delays. One possibility is that local abilities are always expressed at a short-latency delay and integrative abilities are always expressed at a long-latency delay. Alternatively, the neural circuits may be altered over time, leading to a temporal shift in expressing certain abilities; a refractory period could retard integrative responses to a second perturbation, whereas priming could enable integrative responses at short latency. We tested between these three hypotheses in a shoulder muscle by intermixing trials of step torque with either torque pulses ( experiment 1) or double steps of torque ( experiment 2). The second perturbation occurred at 35, 60, and 110 ms after the first perturbation to probe processing throughout the corrective action. The second perturbation reliably evoked short-latency responses in the shoulder muscle linked to only shoulder motion and long-latency responses linked to both shoulder and elbow motion. This pattern is best accounted by the continuous action of controllers with fixed functions. NEW & NOTEWORTHY Sudden displacement of the limb evokes a short-latency reflex, 20-50 ms, based on local muscle stretch and a long-latency reflex based on integrating muscle stretch at different joints. A novel double-perturbation paradigm tested if these abilities are temporally conserved throughout the corrective response or are shifted (retarded or delayed) due to functional changes in the responsible circuits. Multi-joint integration was reliably expressed at a long-latency delay consistent with the continuous operation of circuits with fixed abilities.

Anodal transcranial direct current stimulation does not influence the neural adjustments associated with fatiguing contractions in a hand muscle.

The objective of the current study was to investigate the mechanisms responsible for the briefer time to failure of a submaximal contraction (C2) when performed 60min after a similar contraction (C1), and the influence of anodal transcranial direct current stimulation (a-tDCS) applied over the motor cortex on these mechanisms. In two sessions, ten adults sustained two isometric contractions (35% of maximum) to failure with the abductor pollicis brevis (APB). Before C2, either a-tDCS or sham stimulation was applied over the motor cortex. Fatigue-related changes in Hoffmann (H) and long-latency (LLR) reflexes, motor-evoked potential (MEP) induced by transcranial magnetic stimulation and associated silent period (SP), maximal motor wave (Mmax), voluntary activation (VA), electromyographic (EMG) activity and peak force (PT3) evoked by a 3 pulse-train (100Hz) were investigated. The results indicate that regardless of session, the time to failure was briefer (-13%, p < 0.05) for C2 than C1, with no a-tDCS effect. During C1, MEP amplitude, SP duration and LLR amplitude increased, H-reflex amplitude did not change, and Mmax, VA and PT3 decreased (p < 0.05). Except for EMG activity that was greater during C2 than C1 (p < 0.001), all variables were similar in C1 and C2 (p > 0.05), and recovered their initial values after the 60-min rest, except PT3. The results of the current study indicate that a-tDCS did not influence corticospinal excitability and time to failure of C2 when performed with the APB. These observations may reflect a peripheral origin of the briefer C2 time to failure in the APB.

Pathophysiology of corticobasal degeneration: Insights from neurophysiological studies

BackgroundSeveral studies have applied electrophysiological techniques to physiologically characterize corticobasal degeneration (CBD). MethodsWe performed a systematic literature search of these studies and reviewed all 25 identified articles. ResultsConventional electroencephalography (EEG) is usually normal even in the late stages of disease. Quantitative EEG (qEEG) with spectral analysis revealed mainly lateralized abnormalities, such as an increase of slow wave activity and occasionally the occurrence of sharp waves, and a significant increase of coherence between left parietal-right premotor areas. CBD patients generally have long latency reflexes (LLR) with shorter latencies than in the classic cortical reflex myoclonus observed in progressive myoclonic epilepsy. The somatosensory evoked potentials (SEPs) showed reduced amplitude of the N20–P25 component. These abnormalities may reflect dysfunction of sensory projections to the motor cortex, while the localized parietal cortical damage is thought to be a pivotal factor for the absence of giant SEPs in these patients. Transcranial magnetic stimulation (TMS) revealed asymmetric intracortical disinhibition and asymmetric maps organization; an impaired transcallosal pathways function correlates with the atrophy of the corpus callosum. These findings suggest a pathologic hyperexcitability of the motor cortex, due to a loss of inhibitory input from the sensory cortex. ConclusionsNeurophysiological techniques, in combination with neuroimaging studies, may shed light on the pathophysiological mechanisms of CBD. A better understanding of the disease processes may help clinicians to make a more accurate and early diagnosis. TMS, SEP, LLR, and co-evaluation of EEG and EMG can aid the in differentiation between CBD and other parkinsonism syndromes.

刺激強度の変化が長潜時反射（LLR）の反応性に及ぼす影響

刺激強度の変化が長潜時反射（LLR）の反応性に及ぼす影響

Long-latency reflexes for inter-effector coordination reflect a continuous state feedback controller.

Successful performance in many everyday tasks requires compensating unexpected mechanical disturbance to our limbs and body. The long-latency reflex plays an important role in this process because it is the fastest response to integrate sensory information across several effectors, like when linking the elbow and shoulder or the arm and body. Despite the dozens of studies on inter-effector long-latency reflexes, there has not been a comprehensive treatment of how these reveal the basic control organization that sets constraints on any candidate model of neural feedback control such as optimal feedback control. We considered three contrasting ways that controllers can be organized: multiple independent controllers vs. a multiple-input multiple-output (MIMO) controller, a continuous feedback controller vs. an intermittent feedback controller, and a direct MIMO controller vs. a state feedback controller. Following a primer on control theory and review of the relevant evidence, we conclude that continuous state feedback control best describes the organization of inter-effector coordination by the long-latency reflex.

S159. Long latency reflexes in myoclonic epilepsies

Long latency reflexes (LLRs) are medium to late latency responses which are obtained over a muscle after a peripheral stimulation. In epilepsy, presence and amplitudes are supposed to be higher due to increased cortical excitability. We aimed to analyze LLRs in juvenile myoclonic epilepsy (JME) and progressive myoclonic epilepsy (PME), to determine the frequency of three subtypes and to analyze whether parameters regarding LLRs may be used in differentiating these two disorders. Our hypothesis was cortical excitability and amplitudes and frequency of LLRs would be higher in PME. We included 30 patients with JME, 18 patients with PME and 28 healthy subjects. LLRs were recorded over abductor policis brevis muscle after stimulating median nerve at wrist during rest and active movement. Latencies and amplitudes of segmental reflex and LLRs, presence of LLR I, II, and III, the ratio of segmental reflex amplitude and LLR amplitude were compared among three groups. ROC curves were formed for LLR I amplitude and amplitude ratio to evaluate ‘cut-off’ values in differentiating PME and JME. C reflex was detected in only PME group and LLR I presence during active movement was the highest in PME group (57.9%, p = 0,001). Although LLR I amplitude was also the highest in PME group, ratio was higher in JME group since amplitude of segmental reflex was also higher in patients with PME. Both parameters were higher in PME and JME groups compared to healthy subjects (LLR I amplitude: p = 0.005 and ratio: p = 0.011, Kruskal–Wallis test). LLR I amplitude was able to differentiate patients with epilepsy and healthy subjects with an accuracy of 57–82% (p = 0.008) whereas ratio was able to recognize patients with an accuracy of 60–86% (p = 0.003). Ratio above 1.05 had the sensitivity and specificity of 77.8% and 71%, respectively in diagnosing patients with PME or JME. Presence of C reflex and higher LLR I amplitudes suggest the presence of exaggerated cortical response to peripheral stimuli in PME. However, cortical excitability measured by LLR I amplitude is high in both JME and PME and hence does not provide differentiation of these two disorders.

Effect of arm length and body mass index on abductor pollicis brevis long latency reflex

Background: Long-latency reflex (LLR) is one of the late responses that occur after H-reflex on submaximal stimulation of the mixed nerve. Studies have been done to known the influence of height, arm length, and body mass index (BMI) on nerve conduction study. However, there are hardly studies done to know the effect of arm length and BMI on latency and amplitude of abductor pollicis brevis (APB) LLR among females. Aims and Objective: The objective of the study was to know the effect of arm length and BMI on APB LLR. Materials and Methods: The present cross-sectional study was conducted among 30 healthy adult female volunteers between the age group of 20 and 30 years. LLR recording was done during early follicular phase of the participants using EP/digital nerve conduction/EMG/machine (Recorders and Medicare System, India). LLR was obtained during stimulation of median nerve while abducting the thumb of the dominant hand of the participants. The tabulated data were analyzed using Karl Pearson’s correlation coefficient. Results: Arm length was found to be positively correlated with APB LLR latency and negatively correlated with APB LLR amplitude with r = 0.280 and −0.110, respectively. BMI was found to be negatively correlated with both APB LLR latency and amplitude with r = −0.139 and −0.206, respectively. Conclusion: With increasing arm length, APB H-reflex latency increases, and amplitude decreases. With the increase in BMI, both APB H-reflex latency and amplitude decrease. Hence, arm length and BMI must be taken into consideration while interpreting APB H-reflex among females.

Using Feedback Control to Reduce Limb Impedance during Forceful Contractions

Little is known about the ability to precisely regulate forces or torques during unexpected disturbances, as required during numerous tasks. Effective force regulation implies small changes in force responding to externally imposed displacements, a behavior characterized by low limb impedance. This task can be challenging, since the intrinsic impedance of muscles increases when generating volitional forces. The purpose of this study was to examine the ability to voluntarily reduce limb impedance during force regulation, and the neural mechanisms associated with that ability. Small displacement perturbations were used to quantify elbow impedance during the exertion of volitional elbow torques from 0% to 20% of maximum voluntary contraction. Subjects were instructed either to not intervene with the imposed perturbations or to explicitly intervene so as to minimize the influence of the perturbations on the elbow torque. Our results demonstrated that individuals can reduce the low frequency components of elbow impedance by 35%. Electromyographic analysis suggested that this behavior is mediated by volitional and possibly long-latency reflex pathways with delays of at least 120 ms. These results provide a context for understanding how feedback altered by aging or injuries may influence the ability to regulate forces precisely.

The reliability of commonly used electrophysiology measures

BackgroundElectrophysiological measures can help understand brain function both in healthy individuals and in the context of a disease. Given the amount of information that can be extracted from these measures and their frequent use, it is essential to know more about their inherent reliability. Objective/HypothesisTo understand the reliability of electrophysiology measures in healthy individuals. We hypothesized that measures of threshold and latency would be the most reliable and least susceptible to methodological differences between study sites. MethodsSomatosensory evoked potentials from 112 control participants; long-latency reflexes, transcranial magnetic stimulation with resting and active motor thresholds, motor evoked potential latencies, input/output curves, and short-latency sensory afferent inhibition and facilitation from 84 controls were collected at 3 visits over 24 months at 4 Track-On HD study sites. Reliability was assessed using intra-class correlation coefficients for absolute agreement, and the effects of reliability on statistical power are demonstrated for different sample sizes and study designs. ResultsMeasures quantifying latencies, thresholds, and evoked responses at high stimulator intensities had the highest reliability, and required the smallest sample sizes to adequately power a study. Very few between-site differences were detected. ConclusionsReliability and susceptibility to between-site differences should be evaluated for electrophysiological measures before including them in study designs. Levels of reliability vary substantially across electrophysiological measures, though there are few between-site differences. To address this, reliability should be used in conjunction with theoretical calculations to inform sample size and ensure studies are adequately powered to detect true change in measures of interest.

Whole-body vibration induces distinct reflex patterns in human soleus muscle

The neuronal mechanisms underlying whole body vibration (WBV)-induced muscular reflex (WBV-IMR) are not well understood. To define a possible pathway for WBV-IMR, this study investigated the effects of WBV amplitude on WBV-IMR latency by surface electromyography analysis of the soleus muscle in human adult volunteers. The tendon (T) reflex was also induced to evaluate the level of presynaptic Ia inhibition during WBV. WBV-IMR latency was shorter when induced by low- as compared to medium- or high-amplitude WBV (33.9±5.3msvs. 43.8±3.6 and 44.1±4.2ms, respectively). There was no difference in latencies between T-reflex elicited before WBV (33.8±2.4ms) and WBV-IMR induced by low-amplitude WBV. Presynaptic Ia inhibition was absent during low-amplitude WBV but was present during medium- and high-amplitude WBV. Consequently, WBV induces short- or long-latency reflexes depending on the vibration amplitude. During low-amplitude WBV, muscle spindle activation may induce the short- but not the long-latency WBV-IMR. Furthermore, unlike the higher amplitude WBV, low-amplitude WBV does not induce presynaptic inhibition at the Ia synaptic terminals.

P139 Assessment of cortico-cortical connectivity between premotor and motor cortices by means of combined peripheral nerve electrical stimulation and transcranial magnetic stimulation

Introduction Cortico-cortical connectivity can be assessed by Transcranial Magnetic Stimulation (TMS) paradigms. The “conditioning” coil delivers a pulse over the cortex of interest, followed a few milliseconds later by a pulse delivered on the motor cortex (M1) through the “test” coil. Functional connectivity between the two regions is demonstrated by a change in motor evoked potentials (MEPs) produced by the test coil alone compared to those preceded by conditioning TMS. However, the need to place two TMS coils on the same hemisphere produces practical limitations when testing connectivity between sites located in close spatial proximity to M1 and M1 itself. Objectives Here we devised a new paradigm to test M1 excitability after a TMS conditioning pulse delivered to a different cortical region (in this case the ventral premotor cortex – PMv). We exploited a well-known trans-cortical long latency reflex (LLR) in the upper limb. Therefore, instead of testing MEP amplitudes, we assessed the modulation in amplitude of the LLR by the conditioning TMS pulse. Materials & Methods The LLR was obtained by electrical stimulation of the median nerve at the wrist and recording from the ipsilateral thenar muscles. In some trials the median nerve was stimulated alone, in others it was coupled with a single conditioning TMS pulse delivered to the PMv contralateral to the stimulated hand. The timing of TMS was set from +9 to +42 ms at 3 ms steps after electrical stimulation of the median nerve at the wrist. Results We found a significant effect of conditioning TMS over PMv on the LLR amplitude, only when TMS was delivered around 15 ms from the electrical stimulation. Conclusion We propose that the observed interaction between TMS and peripheral nerve stimulation occurs at the cortical level. In particular, the hypothesis that we favour is that the corticofugal volley evoked by TMS on PMv interacts with the afferent volley from the median nerve at the level of M1. This protocol could provide information on cortico-cortical connectivity in alternative to dual-coil TMS methodology.

Dopaminergic medication unrelated myoclonus is less related to tremor in idiopathic Parkinson's disease.

Myoclonus in Parkinson's disease (PD) may be related or unrelated to dopaminergic medication and may share some features of cortical myoclonus. The aim of this study was to analyze clinical and electrophysiological correlates of the dopaminergic treatment unrelated myoclonus in PD patients. We included 17 PD patients with the end-of-dose myoclonus and 16 PD patients without myoclonus between January 2010 and June 2011. Surface electromyography of upper extremity muscles and long latency reflexes (LLRs) were performed. Positive or negative myoclonus with a duration of 35-100ms was observed. Rest tremor was less frequent in the group with myoclonus. Only one PD patient with myoclonus had C reflex. Mean LLR amplitude was significantly high in PD with myoclonus compared to the group without myoclonus (p=0.024). Dopaminergic treatment unrelated myoclonus is less related to rest tremor in PD, may be positive or negative, and exhibits similar features to cortical myoclonus.

Difference in Cortical Relay Time Between Intrinsic Muscles of Dominant and Nondominant Hands

ABSTRACTThe authors aimed to calculate and compare cortical relay time (CRT) between intrinsic hand muscles and between homonymous muscles of dominant and nondominant hands. The participants comprised 22 healthy volunteers. The CRT for long-latency reflexes (LLRs) was calculated by subtracting the peak latency of somatosensory evoked potentials of component N20 and the onset latency of motor evoked potentials from the onset latency of LLRs. CRT was significantly shorter for the first dorsal interosseous muscle than for the abductor pollicis brevis muscle, regardless of hand dominance. CRT for the abductor pollicis brevis muscle was significantly shorter in the dominant hand than in the nondominant hand. Evaluation of CRT for intrinsic muscles might be beneficial in the understanding of individuated finger functions.

Long-latency Reflexes and Area Measurements of Corpus Callosum in Patients with Multiple Sclerosis

Long-latency Reflexes and Area Measurements of Corpus Callosum in Patients with Multiple Sclerosis

Long-latency reflexes of elbow and shoulder muscles suggest reciprocal excitation of flexors, reciprocal excitation of extensors, and reciprocal inhibition between flexors and extensors

Postural corrections of the upper limb are required in tasks ranging from handling an umbrella in the changing wind to securing a wriggling baby. One complication in this process is the mechanical interaction between the different segments of the arm where torque applied at one joint induces motion at multiple joints. Previous studies have shown the long-latency reflexes of shoulder muscles (50-100 ms after a limb perturbation) account for these mechanical interactions by integrating information about motion of both the shoulder and elbow. It is less clear whether long-latency reflexes of elbow muscles exhibit a similar capability and what is the relation between the responses of shoulder and elbow muscles. The present study utilized joint-based loads tailored to the subjects' arm dynamics to induce well-controlled displacements of their shoulder and elbow. Our results demonstrate that the long-latency reflexes of shoulder and elbow muscles integrate motion from both joints: the shoulder and elbow flexors respond to extension at both joints, whereas the shoulder and elbow extensors respond to flexion at both joints. This general pattern accounts for the inherent flexion-extension coupling of the two joints arising from the arm's intersegmental dynamics and is consistent with spindle-based reciprocal excitation of shoulder and elbow flexors, reciprocal excitation of shoulder and elbow extensors, and across-joint inhibition between the flexors and extensors.

Temporal, but not Directional, Prior Knowledge Shortens Muscle Reflex Latency in Response to Sudden Transition of Support Surface During Walking.

The central nervous system takes advantage of prior knowledge about potential upcoming perturbations for modulating postural reflexes. There are two distinct aspects of prior knowledge: spatial and temporal. This study investigated how each of spatial and temporal prior knowledge contributes to the shortening of muscle response latency. Eleven participants walked on a split-belt treadmill and perturbed by sudden acceleration or deceleration of the right belt at right foot contact. Spatial prior knowledge was given by instruction of possible direction (e.g., only acceleration) of upcoming perturbation at the beginning of an experimental session. Temporal prior knowledge was given to subjects by warning tones at foot contact during three consecutive strides before the perturbation. In response to acceleration perturbation, reflexive muscle activity was observed in soleus (SOL) and gastrocnemius (GAS) muscles. Onset latency of the GAS response was shorter (72 ms vs. 58 ms) when subjects knew the timing of the upcoming perturbation, whereas the latency was independent of directional prior knowledge. SOL onset latency (44 ms) was not influenced by directional nor temporal prior knowledge. Although spinal neural circuit that mediates short-latency reflex was not influenced by the prior knowledge, excitability in supra-spinal neural circuit that mediates medium- and long-latency reflex might be enhanced by knowing the timing of the upcoming perturbation.

Editorial: Plasticity in Multiple Sclerosis: From Molecular to System Level, from Adaptation to Maladaptation.

Editorial: Plasticity in Multiple Sclerosis: From Molecular to System Level, from Adaptation to Maladaptation.

Voluntary reaction time and long-latency reflex modulation.

Stretching a muscle of the upper limb elicits short (M1) and long-latency (M2) reflexes. When the participant is instructed to actively compensate for a perturbation, M1 is usually unaffected and M2 increases in size and is followed by the voluntary response. It remains unclear if the observed increase in M2 is due to instruction-dependent gain modulation of the contributing reflex mechanism(s) or results from voluntary response superposition. The difficulty in delineating between these alternatives is due to the overlap between the voluntary response and the end of M2. The present study manipulated response accuracy and complexity to delay onset of the voluntary response and observed the corresponding influence on electromyographic activity during the M2 period. In all active conditions, M2 was larger compared with a passive condition where participants did not respond to the perturbation; moreover, these changes in M2 began early in the appearance of the response (∼ 50 ms), too early to be accounted for by voluntary overlap. Voluntary response latency influenced the latter portion of M2, with the largest activity seen when accuracy of limb position was not specified. However, when participants aimed for targets of different sizes or performed movements of various complexities, reaction time differences did not influence M2 period activity, suggesting voluntary activity was sufficiently delayed. Collectively, our results show that while a perturbation applied to the upper limbs can trigger a voluntary response at short latency (<100 ms), instruction-dependent reflex gain modulation remains an important contributor to EMG changes during the M2 period.

Increased long-latency reflex activity as a sufficient explanation for childhood hypertonic dystonia: a neuromorphic emulation study

Objective. Childhood dystonia is a movement disorder that interferes with daily movements and can have a devastating effect on quality of life for children and their families. Although injury to basal ganglia is associated with dystonia, the neurophysiological mechanisms leading to the clinical manifestations of dystonia are not understood. Previous work suggested that long-latency stretch reflex (LLSR) is hyperactive in children with hypertonia due to secondary dystonia. We hypothesize that abnormal activity in motor cortices may cause an increase in the LLSR leading to hypertonia. Approach. We modeled two possibilities of hyperactive LLSR by either creating a tonic involuntary drive to cortex, or increasing the synaptic gain in cortical neurons. Both models are emulated using programmable very-large-scale-integrated-circuit hardware to test their sufficiency for producing dystonic symptoms. The emulation includes a joint with two Hill-type muscles, realistic muscle spindles, and 2,304 Izhikevich-type spiking neurons. The muscles are regulated by a monosynaptic spinal pathway with 32 ms delay and a long-latency pathway with 64 ms loop-delay representing transcortical/supra-spinal connections. Main results. When the limb is passively stretched, both models produce involuntary resistance with increased antagonist EMG responses similar to human data; also the muscle relaxation is delayed similar to human data. Both models predict reduced range of motion in voluntary movements. Significance. Although our model is a highly simplified and limited representation of reflex pathways, it shows that increased activity of the LLSR is by itself sufficient to cause many of the features of hypertonic dystonia.