scholarly journals Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat

2016 ◽  
Vol 116 (6) ◽  
pp. 2615-2623 ◽  
Author(s):  
Jessica Pingel ◽  
Jacob Wienecke ◽  
Jakob Lorentzen ◽  
Jens Bo Nielsen
Keyword(s):  
Botulinum Toxin ◽  
Muscle Force ◽  
Botulinum Toxin Injection ◽  
Contralateral Side ◽  
Relative Increase ◽  
Muscle Stiffness ◽  
Triceps Surae ◽  
Reflex Activity ◽  
Muscle Properties ◽  
Triceps Surae Muscle

Botulinum toxin is used with the intention of diminishing spasticity and reducing the risk of development of contractures. Here, we investigated changes in muscle stiffness caused by reflex activity or elastic muscle properties following botulinum toxin injection in the triceps surae muscle in rats. Forty-four rats received injection of botulinum toxin in the left triceps surae muscle. Control measurements were performed on the noninjected contralateral side in all rats. Acute experiments were performed, 1, 2, 4, and 8 wk following injection. The triceps surae muscle was dissected free, and the Achilles tendon was cut and attached to a muscle puller. The resistance of the muscle to stretches of different amplitudes and velocities was systematically investigated. Reflex-mediated torque was normalized to the maximal muscle force evoked by supramaximal stimulation of the tibial nerve. Botulinum toxin injection caused severe atrophy of the triceps surae muscle at all time points. The force generated by stretch reflex activity was also strongly diminished but not to the same extent as the maximal muscle force at 2 and 4 wk, signifying a relative reflex hyperexcitability. Passive muscle stiffness was unaltered at 1 wk but increased at 2, 4, and 8 wk ( P < 0.01). These data demonstrate that botulinum toxin causes a relative increase in reflex stiffness, which is likely caused by compensatory neuroplastic changes. The stiffness of elastic elements in the muscles also increased. The data are not consistent with the ideas that botulinum toxin is an efficient antispastic medication or that it may prevent development of contractures.

scholarly journals Muscle disuse caused by botulinum toxin injection leads to increased central gain of the stretch reflex in the rat

2017 ◽  
Vol 118 (4) ◽  
pp. 1962-1969 ◽  
Author(s):  
Jessica Pingel ◽  
Hans Hultborn ◽  
Lui Näslund-Koch ◽  
Dennis B. Jensen ◽  
Jacob Wienecke ◽  
...  
Keyword(s):  
Botulinum Toxin ◽  
Motor Neurons ◽  
Stretch Reflex ◽  
Botulinum Toxin Injection ◽  
Triceps Surae ◽  
Control Group ◽  
Spinal Motor Neurons ◽  
Spinal Motor ◽  
Triceps Surae Muscle ◽  
Stimulation Of

Botulinum toxin (Btx) is used in children with cerebral palsy and in other neurological patients to diminish spasticity and reduce the risk of development of contractures. We investigated changes in the central gain of the stretch reflex circuitry in response to Btx injection in the triceps surae muscle in rats. Experiments were performed in 21 rats. Eight rats were a control group, and 13 rats were injected with 6 IU of Btx in the left triceps surae muscle. Two weeks after Btx injection, larger monosynaptic reflexes (MSR) were recorded from the left (injected) than the right (noninjected) L4 + L5 ventral roots following stimulation of the corresponding dorsal roots. A similar increase on the left side was observed in response to stimulation of descending motor tracts, suggesting that increased excitability of spinal motor neurons may at least partly explain the increased reflexes. However, significant changes were also observed in postactivation depression of the MSR, suggesting that plastic changes in transmission from Ia afferent to the motor neurons also may be involved. The data demonstrate that muscle paralysis induced by Btx injection is accompanied by plastic adaptations in the central stretch reflex circuitry, which counteract the antispastic effect of Btx. NEW & NOTEWORTHY Injection of botulinum toxin into ankle muscles causes increased gain of stretch reflex. This is caused by adaptive changes in regulation of transmitter release from Ia afferents and increased excitability of spinal motor neurons.

scholarly journals Older Adults Overcome Reduced Triceps Surae Structural Stiffness to Preserve Ankle Joint Quasi-Stiffness During Walking

2020 ◽  
Vol 36 (4) ◽  
pp. 209-216
Author(s):  
Rebecca L. Krupenevich ◽  
William H. Clark ◽  
Gregory S. Sawicki ◽  
Jason R. Franz
Keyword(s):  
Older Adults ◽  
Young Adults ◽  
Achilles Tendon ◽  
Ankle Joint ◽  
Muscle Activation ◽  
Muscle Stiffness ◽  
Triceps Surae ◽  
Triceps Surae Muscle ◽  
Age Related ◽  
Lower Ankle Joint

Ankle joint quasi-stiffness is an aggregate measure of the interaction between triceps surae muscle stiffness and Achilles tendon stiffness. This interaction may be altered due to age-related changes in the structural properties and functional behavior of the Achilles tendon and triceps surae muscles. The authors hypothesized that, due to a more compliant of Achilles’ tendon, older adults would exhibit lower ankle joint quasi-stiffness than young adults during walking and during isolated contractions at matched triceps surae muscle activations. The authors also hypothesized that, independent of age, triceps surae muscle stiffness and ankle joint quasi-stiffness would increase with triceps surae muscle activation. The authors used conventional gait analysis in one experiment and, in another, electromyographic biofeedback and in vivo ultrasound imaging applied during isolated contractions. The authors found no difference in ankle joint quasi-stiffness between young and older adults during walking. Conversely, this study found that (1) young and older adults modulated ankle joint quasi-stiffness via activation-dependent changes in triceps surae muscle length–tension behavior and (2) at matched activation, older adults exhibited lower ankle joint quasi-stiffness than young adults. Despite age-related reductions during isolated contractions, ankle joint quasi-stiffness was maintained in older adults during walking, which may be governed via activation-mediated increases in muscle stiffness.

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