Changes in corticospinal transmission following 8 weeks of ankle joint immobilization
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Changes in corticospinal transmission following 8 weeks of ankle joint immobilization. / Leukel, Christian; Taube, Wolfgang; Rittweger, Jörn; Gollhofer, Albert; Ducos, Michel; Weber, Tobias; Lundbye-Jensen, Jesper.
In: Clinical Neurophysiology, Vol. 126, No. 1, 2015, p. 131-139.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Changes in corticospinal transmission following 8 weeks of ankle joint immobilization
AU - Leukel, Christian
AU - Taube, Wolfgang
AU - Rittweger, Jörn
AU - Gollhofer, Albert
AU - Ducos, Michel
AU - Weber, Tobias
AU - Lundbye-Jensen, Jesper
N1 - CURIS 2015 NEXS 006
PY - 2015
Y1 - 2015
N2 - OBJECTIVES: Joint immobilization has previously been shown to modulate corticospinal excitability. The present study investigated changes in the excitability of distinct fractions of the corticospinal pathway by means of conditioning the H-reflex with transcranial magnetic stimulation (TMS) of the primary motor cortex (Hcond). This method allows assessment of transmission in fast (monosynaptic) and slow(er) (polysynaptic) corticospinal pathways.METHODS: 9 subjects underwent 8weeks of unilateral ankle joint immobilization during daytime, 7 subjects served as controls. The measures obtained before and after immobilization included stretch- and H-reflexes assessing excitability of the spinal reflex circuitries, TMS recruitment curves estimating overall changes in corticospinal excitability, and Hcond.RESULTS: TMS recruitment curves showed an overall increase in corticospinal excitability following immobilization. Importantly, Hcond revealed significant facilitation of conditioned reflexes, but only for longer conditioning intervals, suggesting that immobilization increased excitability only of slower, indirect corticospinal pathways. No changes were observed in the control group. Immobilization had no significant effects on spinal reflex measures.CONCLUSIONS: 8weeks of ankle joint immobilization was accompanied by pathway-specific modulation of corticospinal transmission.SIGNIFICANCE: It is particularly interesting that fast corticospinal projections were unaffected as these are involved in controlling many, if not most, movements in humans.
AB - OBJECTIVES: Joint immobilization has previously been shown to modulate corticospinal excitability. The present study investigated changes in the excitability of distinct fractions of the corticospinal pathway by means of conditioning the H-reflex with transcranial magnetic stimulation (TMS) of the primary motor cortex (Hcond). This method allows assessment of transmission in fast (monosynaptic) and slow(er) (polysynaptic) corticospinal pathways.METHODS: 9 subjects underwent 8weeks of unilateral ankle joint immobilization during daytime, 7 subjects served as controls. The measures obtained before and after immobilization included stretch- and H-reflexes assessing excitability of the spinal reflex circuitries, TMS recruitment curves estimating overall changes in corticospinal excitability, and Hcond.RESULTS: TMS recruitment curves showed an overall increase in corticospinal excitability following immobilization. Importantly, Hcond revealed significant facilitation of conditioned reflexes, but only for longer conditioning intervals, suggesting that immobilization increased excitability only of slower, indirect corticospinal pathways. No changes were observed in the control group. Immobilization had no significant effects on spinal reflex measures.CONCLUSIONS: 8weeks of ankle joint immobilization was accompanied by pathway-specific modulation of corticospinal transmission.SIGNIFICANCE: It is particularly interesting that fast corticospinal projections were unaffected as these are involved in controlling many, if not most, movements in humans.
U2 - 10.1016/j.clinph.2014.04.002
DO - 10.1016/j.clinph.2014.04.002
M3 - Journal article
C2 - 24794515
VL - 126
SP - 131
EP - 139
JO - Clinical Neurophysiology
JF - Clinical Neurophysiology
SN - 1388-2457
IS - 1
ER -
ID: 112902475