Quantitative relations between hypertonia and stretch reflex threshold in spastic hemiparesis

Powers, Randall K.; Marder‐Meyer, J.; Rymer, William Z.

doi:10.1002/ana.410230203

Cited by 201 publications

(106 citation statements)

References 18 publications

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“…The observed impaired modulation in firing rates during voluntary contractions is in contrast to the enhanced excitability of spastic-paretic motoneurons observed at rest (Mottram et al 2009(Mottram et al , 2010. These paradoxical findings are similar to previous observations for enhanced stretch or Hoffman reflexes at rest (Burne et al 2005;Chardon et al 2009;Huang et al 2006;Powers et al 1988), yet not during a background contraction (Burne et al 2005; Thompson et al 2009). We suggest that the enhanced reflex responses at rest in stroke survivors are explained by the presence of a low-level tonic depolarizing synaptic drive to the spastic-paretic motoneuron pool.…”

Section: Role Of Rate Saturation In Reduced Firing Rates Observed In supporting

confidence: 77%

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors

Mottram

Heckman

Powers

et al. 2014

Journal of Neurophysiology

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Mottram CJ, Heckman CJ, Powers RK, Rymer WZ, Suresh NL. Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors. J Neurophysiol 111: 2017-2028, 2014. First published February 26, 2014 doi:10.1152/jn.00389.2013.-Stroke survivors often exhibit abnormally low motor unit firing rates during voluntary muscle activation. Our purpose was to assess the prevalence of saturation in motor unit firing rates in the spastic-paretic biceps brachii muscle of stroke survivors. To achieve this objective, we recorded the incidence and duration of impaired lower-and higherthreshold motor unit firing rate modulation in spastic-paretic, contralateral, and healthy control muscle during increases in isometric force generated by the elbow flexor muscles. Impaired firing was considered to have occurred when firing rate became constant (i.e., saturated), despite increasing force. The duration of impaired firing rate modulation in the lower-threshold unit was longer for spasticparetic (3.9 Ϯ 2.2 s) than for contralateral (1.4 Ϯ 0.9 s; P Ͻ 0.001) and control (1.1 Ϯ 1.0 s; P ϭ 0.005) muscles. The duration of impaired firing rate modulation in the higher-threshold unit was also longer for the spastic-paretic (1.7 Ϯ 1.6 s) than contralateral (0.3 Ϯ 0.3 s; P ϭ 0.007) and control (0.1 Ϯ 0.2 s; P ϭ 0.009) muscles. This impaired firing rate of the lower-threshold unit arose, despite an increase in the overall descending command, as shown by the recruitment of the higher-threshold unit during the time that the lower-threshold unit was saturating, and by the continuous increase in averages of the rectified EMG of the biceps brachii muscle throughout the rising phase of the contraction. These results suggest that impairments in firing rate modulation are prevalent in motor units of spastic-paretic muscle, even when the overall descending command to the muscle is increasing.

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Section: Role Of Rate Saturation In Reduced Firing Rates Observed In supporting

confidence: 77%

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors

Mottram

Heckman

Powers

et al. 2014

Journal of Neurophysiology

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“…Specifically, spinal motoneurons of the finger flexors may have had a lower activation threshold (Lee et al 1987;Powers et al 1988) or were associated with a higher reflex loop gain (Gottlieb et al 1978;Rack et al 1984). Perhaps, muscle spindle signaling properties or activation machinery in the paretic thumb and finger flexors differed, although we could not find support in the literature for either view.…”

Section: Comparison Of Reflex Characteristics Between Thumb and Fingementioning

confidence: 78%

“…Normalized peak torque differences (PTDs) associated with stretches of the paretic thumb muscles were compared with those associated with stretches of the paretic finger muscles (Student's t-test, pairwise, two-tail, ␣ ϭ 0.05) and those associated with stretches of the nonparetic thumb muscles (Student's t-test, two-tail, ␣ ϭ 0.05). Previous studies (Kamper and Rymer 2000;Powers et al 1988) have used PTDs to quantify spastic responses in muscle.…”

Section: Discussionmentioning

confidence: 99%

Lack of Hypertonia in Thumb Muscles After Stroke

Towles

Kamper

Rymer

2010

Journal of Neurophysiology

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Towles JD, Kamper DG, Rymer WZ. Lack of hypertonia in thumb muscles after stroke. J Neurophysiol 104: 2139 -2146, 2010. First published June 28, 2010 doi:10.1152/jn.00423.2009. Despite the importance of the thumb to hand function, little is known about the origins of thumb impairment poststroke. Accordingly, the primary purpose of this study was to assess whether thumb flexors have heightened stretch reflexes (SRs) following stroke-induced hand impairment. The secondary purpose was to compare SR characteristics of thumb flexors in relation to those of finger flexors since it is unclear whether SR properties of both muscle groups are similarly affected poststroke. Stretch reflexes in thumb and finger flexors were assessed at rest on the paretic side in each of 12 individuals with chronic, severe, stroke-induced hand impairment and in the dominant thumb in each of eight control subjects also at rest. Muscle activity and passive joint flexion torques were measured during imposed slow (SS) and fast stretches (FS) of the flexors that span the metacarpophalangeal joints. Putative spasticity was then quantified in terms of the peak difference between FS and SS joint torques and electromyographic changes. For both the hemiparetic and control groups, the mean normalized peak torque differences (PTDs) measured in thumb flexors were statistically indistinguishable (P ϭ 0.57). In both groups, flexor muscles were primarily unresponsive to rapid stretching. For 10 of 12 hemiparetic subjects, PTDs in thumb flexors were less than those in finger flexors (P ϭ 0.03). Paretic finger flexor muscle reflex activity was consistently elicited during rapid stretching. These results may reflect an important difference between thumb and finger flexors relating to properties of the involved muscle afferents and spinal motoneurons.

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“…A similar discrepancy between the resistance to stretch and the level of EMG activity has been described for¯exor muscles of the upper limb in spastic patients. 37,38 Muscle hypertonia in spastic patients is primarily associated with muscle contracture but not with exaggerated re¯exes. 11,27 Muscle tone during functional movements in patients with spastic paresis cannot be explained by an increased activity of motoneurons assessed by EMG recordings.…”

Section: Spastic Gait Disordermentioning

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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Quantitative relations between hypertonia and stretch reflex threshold in spastic hemiparesis

Cited by 201 publications

References 18 publications

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors

Lack of Hypertonia in Thumb Muscles After Stroke

Spastic movement disorder

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