Do Muscle Changes Contribute to the Neurological Disorder in Spastic Paresis?

Background: At the onset of stroke-induced hemiparesis, muscle tissue is normal and motoneurones are not overactive. Muscle contracture and motoneuronal overactivity then develop. Motor command impairments are classically attributed to the neurological lesion, but the role played by muscle changes has not been investigated. Methods: Interaction between muscle and command disorders was explored using quantified clinical methodology-the Five Step Assessment. Six key muscles of each of the lower and upper limbs in adults with chronic poststroke hemiparesis were examined by a single investigator, measuring the angle of arrest with slow muscle stretch (XV1) and the maximal active range of motion against the resistance of the tested muscle (XA). The coefficient of shortening CSH = (XN-XV1)/XN (XN, normally expected amplitude) and of weakness CW = (XV1-XA)/XV1) were calculated to estimate the muscle and command disorders, respectively. Composite CSH (CCSH) and CW (CCW) were then derived for each limb by averaging the six corresponding coefficients. For the shortened muscles of each limb (mean CSH > 0.10), linear regressions explored the relationships between coefficients of shortening and weakness below and above their median coefficient of shortening. Results: A total of 80 persons with chronic hemiparesis with complete lower limb assessments [27 women, mean age 47 (SD 17), time since lesion 8.8 (7.2) years], and 32 with upper limb assessments [18 women, age 32 (15), time since lesion 6.4 (9.3) years] were identified. The composite coefficient of shortening was greater in the lower than in the upper limb (0.12 ± 0.04 vs. 0.08 ± 0.04; p = 0.0002, while the composite coefficient of weakness was greater in the upper limb (0.28 ± 0.12 vs. 0.15 ± 0.06, lower limb; p < 0.0001). In the lower limb shortened muscles, the coefficient of weakness correlated with the composite coefficient of shortening above the 0.15 median CSH (R = 0.43, p = 0.004) but not below (R = 0.14, p = 0.40). Conclusion: In chronic hemiparesis, muscle shortening affects the lower limb particularly, and, beyond a threshold of severity, may alter descending commands. The latter might occur through chronically increased intramuscular tension, and thereby increased muscle afferent firing and activity-dependent synaptic sensitization at the spinal level.

A modified surface EMG biomarker for gait assessment in spastic cerebral palsy.

OBJECTIVE: Muscle clinical metrics are crucial for spastic cocontraction management in children with Cerebral Palsy (CP). We investigated whether the ankle plantar flexors cocontraction index (CCI) normalized with respect to the bipedal heel rise (BHR) approach provides more robust spastic cocontraction estimates during gait than those obtained through the widely accepted standard maximal isometric plantar flexion (IPF). METHODS: Ten control and 10 CP children with equinus gait pattern performed the BHR and IPF testing and walked barefoot 10-m distance. We compared agonist medial gastrocnemius EMG during both testing and CCIs obtained as the ratios of antagonist EMG during swing phase of gait and either BHR or IPF agonist EMG. RESULTS: Agonist EMG values from the BHR were: (i) internally reliable (Cronbach's α = 0.993), (ii) ~50 ± 0.4% larger than IPF, (iii) and positively correlated. Derived CCIs were significantly smaller (p < 0.05) in both populations. CONCLUSION: The bipedal heel rise approach may be accurate enough to reveal greater agonist activity of plantar flexors than the maximal isometric plantar flexion and seems to be more appropriate to obtain cocontraction estimates during swing of gait. SIGNIFICANCE: This modified biomarker may represent a step forward towards improved accuracy of spastic gait management in pediatric.

The neurophysiology of deforming spastic paresis: A revised taxonomy.

This paper revisits the taxonomy of the neurophysiological consequences of a persistent impairment of motor command execution in the classic environment of sensorimotor restriction and muscle hypo-mobilization in short position. Around each joint, the syndrome involves 2 disorders, muscular and neurologic. The muscular disorder is promoted by muscle hypo-mobilization in short position in the context of paresis, in the hours and days after paresis onset: this genetically mediated, evolving myopathy, is called spastic myopathy. The clinician may suspect it by feeling extensibility loss in a resting muscle, although long after the actual onset of the disease. The neurologic disorder, promoted by sensorimotor restriction in the context of paresis and by the muscle disorder itself, comprises 4 main components, mostly affecting antagonists to desired movements: the first is spastic dystonia, an unwanted, involuntary muscle activation at rest, in the absence of stretch or voluntary effort; spastic dystonia superimposes on spastic myopathy to cause visible, gradually increasing body deformities; the second is spastic cocontraction, an unwanted, involuntary antagonist muscle activation during voluntary effort directed to the agonist, aggravated by antagonist stretch; it is primarily due to misdirection of the supraspinal descending drive and contributes to reducing movement amplitude; and the third is spasticity, one form of hyperreflexia, defined by an enhancement of the velocity-dependent responses to phasic stretch, detected and measured at rest (another form of hyperreflexia is "nociceptive spasms", following flexor reflex afferent stimulation, particularly after spinal cord lesions). The 3 main forms of overactivity, spastic dystonia, spastic cocontraction and spasticity, share the same motor neuron hyperexcitability as a contributing factor, all being predominant in the muscles that are more affected by spastic myopathy. The fourth component of the neurologic disorder affects the agonist: it is stretch-sensitive paresis, which is a decreased access of the central command to the agonist, aggravated by antagonist stretch. Improved understanding of the pathophysiology of deforming spastic paresis should help clinicians select meaningful assessments and refined treatments, including the utmost need to preserve muscle tissue integrity as soon as paresis sets in.

Localised sampling of myoelectric activity may provide biased estimates of cocontraction for gastrocnemius though not for soleus and tibialis anterior muscles.

Proper muscle activity quantification is highly relevant to monitor and treat spastic cocontraction. As activity may distribute unevenly within muscle volumes, particularly for pennate calf muscles, surface electromyograms (EMGs) detected by traditional bipolar montage may provide biased estimations of muscle activity. We compared cocontraction estimates obtained using bipolar vs grids of electrodes (high-density EMG, HD-EMG). EMGs were collected from medial gastrocnemius, soleus and tibialis anterior during isometric plantar and dorsi-flexion efforts at three levels (30%, 70% and 100% MVC), knee flexed and extended. Cocontraction index (CCI) was estimated separately for each electrode pair in the grid. While soleus and tibialis anterior CCI estimates did not depend on the detection system considered, for gastrocnemius bipolar electrodes provided larger cocontraction estimates than HD-EMG at highest effort levels, at both knee angles (ANOVA; P < .001). Interestingly, HD-EMG detected greater gastrocnemius EMGs distally during plantar flexions, and greater CCI values proximally during dorsiflexions. These results suggest that bipolar electrodes: (i) provide reliable estimates of soleus and tibialis anterior cocontraction; (ii) may under-or overestimate gastrocnemius cocontraction, depending on their distal or proximal position.

Patterns of upper limb muscle activation in children with unilateral spastic cerebral palsy: Variability and detection of deviations.

BACKGROUND: The aim of this study was two-fold: (1) to quantify the variability of upper limb electromyographic patterns during elbow movements in typically developing children and children with unilateral spastic cerebral palsy, and to compare different amplitude normalization methods; (2) to develop a method using this variability to detect (a) deviations in the patterns of a child with unilateral spastic cerebral palsy from the average patterns of typically developing children, and (b) changes after treatment to reduce muscle activation. METHODS: Twelve typically developing children ([6.7-15.9yo]; mean 11.0 SD 3.0yo) and six children with unilateral spastic cerebral palsy ([7.9-17.4yo]; mean 12.4 SD 4.0yo) attended two sessions during which they performed elbow extension-flexion and pronation-supination movements. Surface electromyography of the biceps, triceps, brachioradialis, pronator teres, pronator quadratus, and brachialis muscles was recorded. The Likelihood method was used to estimate the inter-trial, inter-session, and inter-subject variability of the electromyography patterns for each time point in the movement cycle. Deviations in muscle patterns from the patterns of typically developing children and changes following treatment were evaluated in a case study of a child with cerebral palsy. FINDINGS: Normalization of electromyographic amplitude by the mean peak yielded the lowest variability. The variability data were then used in the case study. This method detected higher levels of activation in specific muscles compared with typically developing children, and a reduction in muscle activation after botulinum toxin A injections. INTERPRETATION: Upper limb surface electromyography pattern analysis can be used for clinical applications in children with cerebral palsy.

Upper Extremity Problem-Solving: Challenging Cases.

Consequences of an upper motor neuron syndrome (UMNS) include voluntary weakness or paresis, superimposed involuntary phenomena such as spastic co-contraction and associated reactions, and superimposed rheologic changes in affected muscles. This article describes the use of dynamic poly-electromyography to assess UMNS muscle overactivity and inform muscle selection for chemodenervation. Cases are presented that involve spastic co-contraction, spastic dystonia, associated reactions, hyperextended wrist and finger flexor tenodesis, differentiating neural versus non-neural (rheologic) hypertonia, upper motor neuron weakness, muscle selection for chemodenervation, and electrical stimulation for muscle specific targeting.

Coefficients of impairment in deforming spastic paresis.

This position paper introduces an assessment method using staged calculation of coefficients of impairment in spastic paresis, with its rationale and proposed use. The syndrome of deforming spastic paresis superimposes two disorders around each joint: a neural disorder comprising stretch-sensitive paresis in agonists and antagonist muscle overactivity, and a muscle disorder ("spastic myopathy") combining shortening and loss of extensibility in antagonists. Antagonist muscle overactivity includes spastic cocontraction (misdirected descending command), spastic dystonia (tonic involuntary muscle activation, at rest) and spasticity (increased velocity-dependent reflexes to phasic stretch, at rest). This understanding of various types of antagonist resistance as the key limiting factors in paretic movements prompts a stepwise, quantified, clinical assessment of antagonist resistances, elaborating on the previously developed Tardieu Scale. Step 1 quantifies limb function (e.g. ambulation speed in lower limb, Modified Frenchay Scale in upper limb). The following four steps evaluate various angles X of antagonist resistance, in degrees all measured from 0°, position of minimal stretch of the tested antagonist. Step 2 rates the functional muscle length, termed XV1 (V1, slowest stretch velocity possible), evaluated as the angle of arrest upon slow and strong passive muscle stretch. XV1 is appreciated with respect to the expected normal passive amplitude, XN, and reflects combined muscle contracture and residual spastic dystonia. Step 3 determines the angle of catch upon fast stretch, termed XV3 (V3, fastest stretch velocity possible), reflecting spasticity. Step 4 measures the maximal active range of motion against the antagonist, termed XA, reflecting agonist capacity to overcome passive (stiffness) and active (spastic cocontraction) antagonist resistances over a single movement. Finally, Step 5 rates the residual active amplitude after 15 seconds of maximal amplitude rapid alternating movements, XA15. Amplitude decrement from XA to XA15 reflects fatigability. Coefficients of shortening (XN-XV1)/XN, spasticity (XV1-XV3)/XV1, weakness (XV1-XA)/XV1 and fatigability (XA-XA15)/XA are derived. A high (e.g., >10%) coefficient of shortening prompts aggressive treatment of the muscle disorder--e.g., by stretch programs, such as prolonged stretch postures -, while high coefficients of weakness or fatigability prompt addressing the neural motor command disorder, e.g. using training programs such as repeated alternating movements of maximal amplitude.