Chronic transformation of muscle in spasticity: a peripheral contribution to increased tone.

Hufschmidt, Andreas; Mauritz, Karl Heinz

doi:10.1136/jnnp.48.7.676

Cited by 257 publications

(106 citation statements)

References 27 publications

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“…Torque motor experiments applied to upper and lower limb muscles indicate a major, non-re¯ex contribution to the spastic muscle tone in the antigravity muscles, ie, in the leg extensors and elbow¯exors. 42,43 Histochemistry and morphometry studies of spastic muscle have revealed neurogenic changes of the muscle ®bres. 14,36 These include: (a) increased levels of muscle ®bre atrophy (especially of type II ®bres); (b) a predominance of type I ®bres in the gastrocnemius during later stages, when spasticity of cerebral origin has been established; (c) structural changes, such as the appearance of target ®bres, mainly in type I ®bres and (d) a signi®cant part of changes of mechanical muscle ®bre properties may be attributed to a shortening of muscle length as a result of a decrease in the number of sarcomeres in series along the myo®brils accompanied by an increase in resistance to stretch.…”

Section: Motor Unit Transformation and Spastic Muscle Tonementioning

confidence: 99%

Spastic movement disorder

Dietz¹

2000

Spinal Cord

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This review deals with the neuronal mechanisms underlying spastic movement disorder, assessed by electrophysiological means with the aim of ®rst, a better understanding of the underlying pathophysiology and second, the selection of an adequate treatment. For the patient usually one of the ®rst symptoms of a lesion within the central motor system represents the movement disorder, which is most characteristic during locomotion in patients with spasticity. The clinical examination reveals exaggerated tendon tap re¯exes and increased muscle tone typical of the spastic movement disorder. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms being in operation during an active movement. By the recording and analysis of electrophysiological and biomechanical parameters during a functional movement such as locomotion, the signi®cance of, for example, impaired re¯ex behaviour or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and signi®cance of the mechanisms underlying the disorder of functional movement which impairs the patient. Spinal Cord (2000) 38, 389 ± 393

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Section: Motor Unit Transformation and Spastic Muscle Tonementioning

confidence: 99%

Spastic movement disorder

Dietz¹

2000

Spinal Cord

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“…"Easy-todifficult" sequence in terms of progressively decreasing robotic support, determined by stiffness setting: K (Nm/rad), is same for each visit throughout training, but task difficulty in terms of vertical location of targets (challenging AROM) and speed of targets (challenging speed of ankle targeting) on screen are adjusted in weeks 3-4 and 5-6, respectively, based on prior subject performance in order to provide challenge where applicable (at least sustained 80% targeting success without robotic assistance in weeks 1 and 2) and sustain subject motivation. and ramp down) was to avoid evoking stretch reflex, as reported in other studies [15,19,[34][35]. Under the relaxed condition, subjects experienced a series of perturbations during which the ankle was stretched to a commanded position, held at steady state for 1 s, and returned to neutral.…”

Section: Stiffness Measurementmentioning

confidence: 99%

“…In fact, the manifestation of increased motor neuron excitability and an increased resistance to passive movement have been observed in clinical assessments [14][15][16][17][18]. In addition, structural changes of muscle fibers and connective tissue may contribute to alterations in the intrinsic mechanical properties, e.g., stiffness of a joint.…”

Section: Introductionmentioning

confidence: 99%

Changes in passive ankle stiffness and its effects on gait function in people with chronic stroke

Roy¹,

Forrester²,

Macko³

et al. 2013

JRRD

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Abstract-Mechanical impedance of the ankle is known to influence key aspects of ankle function. We investigated the effects of robot-assisted ankle training in people with chronic stroke on the paretic ankle's passive stiffness and its relationship to overground gait function. Over 6 wk, eight participants with residual hemiparetic deficits engaged in a visuomotor task while seated that required dorsiflexion (DF) or plantar flexion (PF) of their paretic ankle with an ankle robot ("anklebot") assisting as needed. Passive ankle stiffness (PAS) was measured in both the trained sagittal and untrained frontal planes. After 6 wk, the PAS decreased in both DF and PF and reverted into the variability of age-matched controls in DF. Changes in PF PAS correlated strongly with gains in paretic step lengths (Spearman rho = 0.88, p = 0.03) and paretic stride lengths (Spearman rho = 0.82, p = 0.05) during independent floor walking. Moreover, baseline PF PAS were correlated with gains in paretic step lengths (Spearman rho = 0.94, p = 0.01), paretic stride lengths (Spearman rho = 0.83, p = 0.05), and singlesupport stance duration (Spearman rho = 0.94, p = 0.01); and baseline eversion PAS were correlated with gains in cadence (Spearman rho = 0.88, p = 0.03). These findings suggest that ankle robot-assisted, visuomotor-based, isolated ankle training has a positive effect on paretic ankle PAS that strongly influences key measures of gait function.

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“…The effect of disuse of the peripheral motor apparatus could be excluded, because all patients in this study walked independently and were on a series of therapeutic exercises, and moreover, TLT of their non-affected side was not different from that of the normal subjects. Hufschmidt and Mauritz (1985) reported that the enhancement in elastic and plastic resistance of the spastic muscle. Such changes, however, occurred more than one year after the onset of disease in their study.…”

Section: Discussionmentioning

confidence: 99%

The altered time course of tension development during the initiation of fast movement in hemiplegic patients.

Tsuji

Nakamura

1987

Tohoku J. Exp. Med.

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Med., 1987, 151(2), 137-143 The time course of tension development produced by fast isometric contraction of the quadriceps femoris muscle for knee extension was examined on eight normal subjects and 14 patients with spastic hemiparesis due to stroke. Tension lag time (TLT), the latency from the onset of EMG activities to the rise of tension, and contraction time (FTmax), the period from the rise of tension to its maximum, were longer in the patients than in the normal subjects. The prolongation of FTmax correlated with the decreased rate of tension development. The results indicated that the temporal characteristics of tension development altered in the spastic paresis, reflecting functional changes in the muscle and motor neurons.rapid force generation ; time course ; spastic muscle Recent studies have indicated that the temporal profile of the muscular contraction during the initiation of fast movement was altered in patients with spastic paresis. For instance, the duration of the first burst activity of the agonist muscle in a ballistic movement was prolonged in patients with cerebral hemiparesis (Angel 1975) and in those with amyotrophic lateral sclerosis (Hallett 1976). Electromyographic (EMG) summation time or motor time, a latency from the onset of EMG activities of a prime mover muscle to the initiation of an actual movement in a reaction time study, was long in patients with cerebral hemiparesis compared to normal subjects (Jung and Dietz 1975;Nakamura and Taniguchi 1977). However, the direct measurement of the force output was not performed in these studies, and the relationship between the force output and its time course during the initiation of the fast movements has not been fully examined.Our previous studies (Nakamura et al. 1984;Nagasaki and Nakamura 1985) have shown that the motor time is composed of two consecutive phases ; the tension lag and the tension-developing phase. The former is a latency from the onset of EMG activities to the rise of tension. The latter is a period for real development of tension to overcome the load of the body segment to be moved.

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Chronic transformation of muscle in spasticity: a peripheral contribution to increased tone.

Cited by 257 publications

References 27 publications

Spastic movement disorder

Spastic movement disorder

Changes in passive ankle stiffness and its effects on gait function in people with chronic stroke

The altered time course of tension development during the initiation of fast movement in hemiplegic patients.

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