Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat
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Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat. / Pingel, Jessica; Wienecke, Jacob; Lorentzen, Jakob; Nielsen, Jens Bo.
In: Journal of Neurophysiology, Vol. 116, No. 6, 2016, p. 2615-2623.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat
AU - Pingel, Jessica
AU - Wienecke, Jacob
AU - Lorentzen, Jakob
AU - Nielsen, Jens Bo
N1 - CURIS 2016 NEXS 361
PY - 2016
Y1 - 2016
N2 - Botulinum toxin is used to diminish spasticity and reduce 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 non-injected contralateral side in all rats. Acute experiments were performed 1, 2, 4 and 8 weeks following injection. The triceps surae muscle was dissected free, 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 (Mmax) 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 Mmax at 2 and 4 weeks, signifying a relative reflex hyperexcitability. Passive muscle stiffness was unaltered at 1 week, but increased at 2, 4 and 8 weeks (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.
AB - Botulinum toxin is used to diminish spasticity and reduce 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 non-injected contralateral side in all rats. Acute experiments were performed 1, 2, 4 and 8 weeks following injection. The triceps surae muscle was dissected free, 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 (Mmax) 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 Mmax at 2 and 4 weeks, signifying a relative reflex hyperexcitability. Passive muscle stiffness was unaltered at 1 week, but increased at 2, 4 and 8 weeks (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.
KW - Faculty of Science
KW - Botulinum toxin
KW - Muscle stiffness
KW - Plasticity
KW - Reflex
KW - Spinal cord
U2 - 10.1152/jn.00452.2016
DO - 10.1152/jn.00452.2016
M3 - Journal article
C2 - 27628204
VL - 116
SP - 2615
EP - 2623
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 6
ER -
ID: 166273380