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Stretch Reflexes (stretch + reflex)

Distribution by Scientific Domains

Life Sciences	75%
Medical Sciences	25%

Selected Abstracts

Phase-dependent and task-dependent modulation of stretch reflexes during rhythmical hand tasks in humans

THE JOURNAL OF PHYSIOLOGY, Issue 3 2005
Ruiping Xia
Phase-dependent and task-dependent modulation of reflexes has been extensively demonstrated in leg muscles during locomotory activity. In contrast, the modulation of reflex responses of hand muscles during rhythmic movement is poorly documented. The objective of this study was to determine whether comparable reflex modulation occurs in muscles controlling finger motions during rhythmic, fine-motor tasks akin to handwriting. Twelve healthy subjects performed two rhythmic tasks while reflexes were evoked by mechanical perturbations applied at various phases of each task. Electromyograms (EMGs) were recorded from four hand muscles, and reflexes were averaged during each task relative to the movement phase. Stretch reflexes in all four muscles were found to be modulated in amplitude with respect to the phase of the rhythmic tasks, and also to vary distinctly with the tasks being conducted. The extent and pattern of reflex modulation differed between muscles in the same task, and between tasks for the same muscle. Muscles with a primary role in each task showed a higher correlation between reflex response and background EMG than other muscles. The results suggest that the modulation patterns observed may reflect optimal strategies of central,peripheral interactions in controlling the performance of fine-motor tasks. As with comparable studies on locomotion, the phase-dependency of the stretch reflexes implies a dynamically fluctuating role of proprioceptive feedback in the control of the hand muscles. The clear task-dependency is also consistent with a dynamic interaction of sensory feedback and central programming, presumably adapted to facilitate the successful performance of the different fine-motor tasks. [source]

Improved organotypic cell culture model for analysis of the neuronal circuit involved in the monosynaptic stretch reflex

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2006
Björn Dagberg
Abstract Knowledge regarding neuronal circuit formation is central for the understanding of the vast network making up the brain. It is therefore necessary to find novel ways to analyze the mechanisms involved in well-defined neural circuits. We present an improved in vitro model of the monosynaptic stretch reflex circuit, based on primary organotypic cell cultures. By using limb tissue as a source of muscle fibers instead of circumspinal tissue we could make the in vitro system more in vivo like in the sense that it focuses on the stretch reflex involving limb muscles. Furthermore, our analyses showed that this procedure allows muscle fibers to follow the normal developmental pattern. Particularly interesting was the finding of slow tonic myosin heavy chain expressing muscle fibers, a developmental marker for muscle spindles, in the cultures showing that this system has the potential to contain the complete reflex circuits. © 2006 Wiley-Liss, Inc. [source]

Mechanical and neural stretch responses of the human soleus muscle at different walking speeds

THE JOURNAL OF PHYSIOLOGY, Issue 13 2009
Neil J. Cronin
During human walking, a sudden trip may elicit a Ia afferent fibre mediated short latency stretch reflex. The aim of this study was to investigate soleus (SOL) muscle mechanical behaviour in response to dorsiflexion perturbations, and to relate this behaviour to short latency stretch reflex responses. Twelve healthy subjects walked on a treadmill with the left leg attached to an actuator capable of rapidly dorsiflexing the ankle joint. Ultrasound was used to measure fascicle lengths in SOL during walking, and surface electromyography (EMG) was used to record muscle activation. Dorsiflexion perturbations of 6 deg were applied during mid-stance at walking speeds of 3, 4 and 5 km h,1. At each walking speed, perturbations were delivered at three different velocities (slow: ,170 deg s,1, mid: ,230 deg s,1, fast: ,280 deg s,1). At 5 km h,1, fascicle stretch amplitude was 34,40% smaller and fascicle stretch velocity 22,28% slower than at 3 km h,1 in response to a constant amplitude perturbation, whilst stretch reflex amplitudes were unchanged. Changes in fascicle stretch parameters can be attributed to an increase in muscle stiffness at faster walking speeds. As stretch velocity is a potent stimulus to muscle spindles, a decrease in the velocity of fascicle stretch at faster walking speeds would be expected to decrease spindle afferent feedback and thus stretch reflex amplitudes, which did not occur. It is therefore postulated that other mechanisms, such as altered fusimotor drive, reduced pre-synaptic inhibition and/or increased descending excitatory input, acted to maintain motoneurone output as walking speed increased, preventing a decrease in short latency reflex amplitudes. [source]

Interaction of pre-programmed control and natural stretch reflexes in human landing movements

THE JOURNAL OF PHYSIOLOGY, Issue 3 2002
Martin J. N. McDonagh
Pre-programmed mechanisms of motor control are known to influence the gain of artificially evoked stretch reflexes. However, their interaction with stretch reflexes evoked in the context of unimpeded natural movement is not understood. We used a landing movement, for which a stretch reflex is an integral part of the natural action, to test the hypothesis that unpredicted motor events increase stretch reflex gain. The unpredicted event occurred when a false floor, perceived to be solid, collapsed easily on impact, allowing the subjects to descend for a further 85 ms to a solid floor below. Spinal stretch reflexes were measured following solid floor contact. When subjects passed through the false floor en route to the solid floor, the amplitude of the EMG reflex activity was double that found in direct falls. This was not due to differences in joint rotations between these conditions. Descending pathways can modify H- and stretch-reflex gain in man. We therefore manipulated the time between the false and real floor contacts and hence the time available for transmission along these pathways. With 30 ms between floors, the enhancement of the reflex was extinguished, whereas with 50 ms between floors it reappeared. This excluded several mechanisms from being responsible for the doubling of the reflex EMG amplitude. It is argued that the enhanced response is due to the modulation of reflex gain at the spinal level by signals in descending pathways triggered by the false platform. The results suggest the future hypothesis that this trigger could be the absence of afferent signals expected at the time of false floor impact and that salient error signals produced from a comparison of expected and actual sensory events may be used to reset reflex gains. [source]

The pathophysiology of spasticity

EUROPEAN JOURNAL OF NEUROLOGY, Issue 2002
G. Sheean
Spasticity is only one of several components of the upper motor neurone (UMN) syndrome, known collectively as the `positive' phenomena, that are characterized by muscle overactivity. Other components include tendon hyper-reflexia, clonus, the clasp-knife phenomenon, flexor and extensor spasms, a Babinski sign, and spastic dystonia. Spasticity is a form of hypertonia due to hyperexcitable tonic stretch reflexes. It is distinguished from rigidity by its dependence upon the speed of the muscle stretch and by the presence of other positive UMN signs. Hyperactive spinal reflexes mediate most of these positive phenomena, while others are due to disordered control of voluntary movement or abnormal efferent drive. An UMN lesion disturbs the balance of supraspinal inhibitory and excitatory inputs, producing a state of net disinhibition of the spinal reflexes. These include proprioceptive (stretch) and nociceptive (flexor withdrawal and extensor) reflexes. The clinical syndrome resulting from an UMN lesion depends more upon its location and extent, and the time since it occurred, than on the pathology of the lesion. However, the change in spinal reflex excitability cannot simply be due to an imbalance in supraspinal control. The delayed onset after the lesion and the frequent reduction in reflex excitability over time, suggests plasticity in the central nervous system. Knowledge of the electrophysiology and neurochemistry of spinal reflexes, together with the action of antispasticity drugs, helps us to understand the pathophysiology of spasticity. [source]

Guillain,Barré syndrome in childhood

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5-6 2005
Monique M Ryan
Abstract:, The Guillain,Barré syndrome (GBS) is characterized by the acute onset of rapidly progressive, symmetric muscle weakness with absent or decreased muscle stretch reflexes. GBS is the most common cause of acute flaccid paralysis in childhood, with an incidence in Australia of 0.8 per 100 000 children per year. Recent advances in this field have included identification of a number of clinical and neurophysiologic subtypes of GBS, enabling improved characterization of etiology and improved prognostication in this disorder. [source]

Sensorimotor integration in movement disorders

MOVEMENT DISORDERS, Issue 3 2003
Giovanni Abbruzzese MD
Abstract Although current knowledge attributes movement disorders to a dysfunction of the basal ganglia,motor cortex circuits, abnormalities in the peripheral afferent inputs or in their central processing may interfere with motor program execution. We review the abnormalities of sensorimotor integration described in the various types of movement disorders. Several observations, including those of parkinsonian patients' excessive reliance on ongoing visual information during movement tasks, suggest that proprioception is defective in Parkinson's disease (PD). The disturbance of proprioceptive regulation, possibly related to the occurrence of abnormal muscle-stretch reflexes, might be important for generating hypometric or bradykinetic movements. Studies with somatosensory evoked potentials (SEPs), prepulse inhibition, and event-related potentials support the hypothesis of central abnormalities of sensorimotor integration in PD. In Huntington's disease (HD), changes in SEPs and long-latency stretch reflexes suggest that a defective gating of peripheral afferent input to the brain might impair sensorimotor integration in cortical motor areas, thus interfering with the processing of motor programs. Defective motor programming might contribute to some features of motor impairment in HD. Sensory symptoms are frequent in focal dystonia and sensory manipulation can modify the dystonic movements. In addition, specific sensory functions (kinaesthesia, spatial,temporal discrimination) can be impaired in patients with focal hand dystonia, thus leading to a "sensory overflow." Sensory input may be abnormal and trigger focal dystonia, or defective "gating" may cause an input,output mismatch in specific motor programs. Altogether, several observations strongly support the idea that sensorimotor integration is impaired in focal dystonia. Although elemental sensation is normal in patients with tics, tics can be associated with sensory phenomena. Some neurophysiological studies suggest that an altered "gating" mechanism also underlies the development of tics. This review underlines the importance of abnormal sensorimotor integration in the pathophysiology of movement disorders. Although the physiological mechanism remains unclear, the defect is of special clinical relevance in determining the development of focal dystonia. [source]