Spasticity in adults with cerebral palsy and multiple sclerosis measured by objective clinically applicable technique

Yamaguchi, Tomohiko; Petersen, Tue Hvass; Kirk, Henrik; Forman, Christian Riis; Svane, Christian; Kofoed-Hansen, Mathilde; Boesen, Finn; Lorentzen, Jakob

doi:10.1016/j.clinph.2018.07.004

Cited by 29 publications

(26 citation statements)

References 40 publications

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“…Data are then transferred to a computer via Bluetooth. The technical properties of the device are explained more thoroughly in Yamaguchi et al (2018) .…”

Section: Methodsmentioning

confidence: 99%

Sustained involuntary muscle activity in cerebral palsy and stroke: same symptom, diverse mechanisms

Forman

Svane

Kruuse

et al. 2019

Brain Communications

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Abstract Individuals with lesions of central motor pathways frequently suffer from sustained involuntary muscle activity. This symptom shares clinical characteristics with dystonia but is observable in individuals classified as spastic. The term spastic dystonia has been introduced, although the underlying mechanisms of involuntary activity are not clarified and vary between individuals depending on the disorder. This study aimed to investigate the nature and pathophysiology of sustained involuntary muscle activity in adults with cerebral palsy and stroke. Seventeen adults with cerebral palsy (Gross Motor Function Classification System I–V), 8 adults with chronic stroke and 14 control individuals participated in the study. All individuals with cerebral palsy or stroke showed increased resistance to passive movement with Modified Ashworth Scale >1. Two-minute surface EMG recordings were obtained from the biceps muscle during attempted rest in three positions of the elbow joint; a maximally flexed position, a 90-degree position and a maximally extended position. Cross-correlation analysis of sustained involuntary muscle activity from individuals with cerebral palsy and stroke, and recordings of voluntary isometric contractions from control individuals were performed to examine common synaptic drive. In total, 13 out of 17 individuals with cerebral palsy and all 8 individuals with stroke contained sustained involuntary muscle activity. In individuals with cerebral palsy, the level of muscle activity was not affected by the joint position. In individuals with stroke, the level of muscle activity significantly (P < 0.05) increased from the flexed position to the 90 degree and extended position. Cumulant density function indicated significant short-term synchronization of motor unit activities in all recordings. All groups exhibited significant coherence in the alpha (6–15 Hz), beta (16–35 Hz) and early gamma band (36–60 Hz). The cerebral palsy group had lower alpha band coherence estimates, but higher gamma band coherence estimates compared with the stroke group. Individuals with increased resistance to passive movement due to cerebral palsy or stroke frequently suffer sustained involuntary muscle activity, which cannot exclusively be described by spasticity. The sustained involuntary muscle activity in both groups originated from a common synaptic input to the motor neuron pool, but the generating mechanisms could differ between groups. In cerebral palsy it seemed to originate more from central mechanisms, whereas peripheral mechanisms likely play a larger role in stroke. The sustained involuntary muscle activity should not be treated simply like the spinal stretch reflex mediated symptom of spasticity and should not either be treated identically in both groups.

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“…Data are then transferred to a computer via Bluetooth. The technical properties of the device are explained more thoroughly in Yamaguchi et al (2018) .…”

Section: Methodsmentioning

confidence: 99%

Sustained involuntary muscle activity in cerebral palsy and stroke: same symptom, diverse mechanisms

Forman

Svane

Kruuse

et al. 2019

Brain Communications

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“…A number of other studies have similarly failed to demonstrate exaggerated reflexes using objective biomechanical and electrophysiological techniques in patients, who have been diagnosed clinically with spasticity due to multiple sclerosis (Mirbagheri et al, 2008;Lorentzen et al, 2010;Zhang et al, 2014), stroke (Mirbagheri et al, 2008;Lorentzen et al, 2010), spinal cord injury (Lorentzen et al, 2010), or CP (Yamaguchi et al, 2018). As pointed out in several of these studies one explanation may be that it is difficult as part of the neurological examination to distinguish whether pathologically increased resistance to movement of a joint is caused by exaggerated reflex (neural) activity or (non-neural) changes in the elastic elements in the muscle, tendon, joint and connective tissue around the joint.…”

Section: Discussionmentioning

confidence: 99%

“…Computer-controlled perturbations using an electromotor as in the present study, guarantees that sufficiently high velocities are reached, but this may not be the case in the clinic where the examiner only have their own ability to generate explosive force to rely on. This emphasizes the need of more precise objective measurement of spasticity in individuals with CP when initially determining the need for anti-spasticity medication and monitoring change in the relative contribution of hyperexcitability and passive resistance from childhood to adulthood (Lorentzen et al, 2012;Bar-On et al, 2014a,b;Yamaguchi et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies using objective electrophysiological and biomechanical techniques have indicated that it is reduced central neural drive, reduced muscle mass and altered muscle mechanics, including increased passive (non-neural) stiffness leading to reduced joint mobility (contractures) and joint deformities, which are the main causes of limited functional capacity and reduced gait ability in the group of ambulant (high-functioning) adults with CP (Geertsen et al, 2015;Gillett et al, 2018;Yamaguchi et al, 2018;Frisk et al, 2019a,b). In contrast, hyperexcitability of stretch reflexes and muscle "overactivity" appear to have no or little significance (Geertsen et al, 2015;Frisk et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Increased Ankle Plantar Flexor Stiffness Is Associated With Reduced Mechanical Response to Stretch in Adults With CP

Lorentzen

Frisk

Nielsen

et al. 2021

Front. Bioeng. Biotechnol.

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Hyperexcitable stretch reflexes are often not present despite of other signs of spasticity in people with brain lesion. Here we looked for evidence that increased resistance to length change of the plantar flexor muscle-fascicles may contribute to a reduction in the stretch reflex response in adults with cerebral palsy (CP). A total of 17 neurologically intact (NI) adults (mean age 36.1; 12 female) and 13 ambulant adults with CP (7 unilateral; mean age 33.1; 5 female) participated in the study. Subjects were seated in a chair with the examined foot attached to a foot plate, which could be moved by a computer-controlled electromotor. An ultrasound probe was placed over the medial aspect of the leg to measure the length of medial gastrocnemius muscle fascicles. Slow (7 deg/s) and fast (200 deg/s) stretches with amplitude 6 deg of the plantar flexors were applied over an ankle range of 70 deg at 10 deg intervals between 60 and 130 deg plantarflexion. It was checked by EMG electrodes that the slow stretches were sufficiently slow not to elicit any activity and that the fast stretches were sufficiently quick to elicit a maximal stretch reflex in both groups. The torque elicited by the stretches was measured together with changes in the length of medial gastrocnemius muscle fascicles. Muscle fascicles increased significantly in length with increasing dorsiflexion position in both populations (p < 0.001), but the fascicles were shorter in the CP population at all positions. Slow stretches elicited significantly larger torque and significantly smaller length change of muscle fascicles as the ankle joint position was moved more towards dorsiflexion in CP than in NI (p < 0.001). Fast stretches elicited larger torque responses at ankle joint positions of 80–100 deg in the NI than in the CP group (p < 0.01). A significant negative correlation was observed between the torque response and muscle fascicle length change to slow stretch in CP (p < 0.05), but not in NI. These findings support that increased passive resistance of the ankle plantar flexor muscle-tendon unit and development of contractures may conceal stretch reflex response in adults with CP. We argue that this should be taken into account in the neurological examination of spasticity.

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“…To estimate the resistance torque of the time-dependent part, which is of energy loss quality, we can use the following equation at a certain angular velocity θ · : 23,28…”

Section: Methodsmentioning

confidence: 99%

Modeling the resistance mechanism of passive knee joint flexion and extension for use in rehabilitation equipment

Amiri

Ghomsheh

Ghazalian

2021

Proc Inst Mech Eng H

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The purpose of this study was to model the resistance mechanism of Passive Knee Joint Flexion and Extension to create a similar torque mechanism in rehabilitation equipment. In order to better model the behavior of passive knee tissues, it is necessary to exactly calculate the two coefficients of elasticity of time-independent and time-dependent parts. Ten healthy male volunteers (mean height 176.4+/−4.59 cm) participated in this study. Passive knee joint flexion and extension occurred at velocities of 15, 45, and 120 (degree/s), and in five consecutive cycles and within the range of 0 to 100° of knee movement on the sagittal plane on Cybex isokinetic dynamometer. To ensure that the muscles were relaxed, the electrical activity of knee muscles was recorded. The elastic coefficient, (KS) increased with elevating the passive velocity in flexion and extension. The elastic coefficient, (KP) was observed to grow with the passive velocity increase. While, the viscous coefficient (C) diminished with passive velocity rise in extension and flexion. The heightened passive velocity of the motion resulted in increased hysteresis (at a rate of 42%). The desired of passive velocity is lower so that there is less energy lost and the viscoelastic resistance of the tissue in the movement decreases. The Coefficient of Determination, R2 between the model-responses and experimental curves in the extension was 0.96 < R2 < 0.99 and in flexion was 0.95 < R2 < 0.99. This modeling is capable of predicting the true performance of the components of passive knee movement and we can create a resistance mechanism in the rehabilitation equipment to perform knee joint movement. Quantitative measurements of two elastic coefficients of Time-independent and Time-dependent parts passive knee joint coefficients should be used for better accurate simulation the behavior of passive tissues in the knee which is not seen in other studies.

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Spasticity in adults with cerebral palsy and multiple sclerosis measured by objective clinically applicable technique

Cited by 29 publications

References 40 publications

Sustained involuntary muscle activity in cerebral palsy and stroke: same symptom, diverse mechanisms

Sustained involuntary muscle activity in cerebral palsy and stroke: same symptom, diverse mechanisms

Increased Ankle Plantar Flexor Stiffness Is Associated With Reduced Mechanical Response to Stretch in Adults With CP

Modeling the resistance mechanism of passive knee joint flexion and extension for use in rehabilitation equipment

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