| Project/Area Number |
05454263
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | TOKYO METROPOLITAN INSTITUTE FOR NEUROSCIENCES |
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Principal Investigator |
TANAKA Reisaku Tokyo Metropolitan Inst.For Neurosciences, 病態神経生理学研究部門, 参事研究員 (20003626)
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| Co-Investigator(Kenkyū-buntansha) |
KAGAMIHARA Yasuhiro Tokyo Metropolitan Inst.For Neurosciences, 病態神経生理学研究部門, 兼務研究員 (50146784)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 1994: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Spasticity / Ankle movements / H-reflex / Reciprocal inhibition / Ia inhibition / Soleus muscle / Pretibial muscle / Man / 脊髄疾患 / 足背屈運動 |
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| Research Abstract |
The present research aimed at revealing neurophysiological mechanisms underlying spasticity, in terms of disorders in spinal reflex activities concerning myotatic reflex and reciprocal inhibition upon initiation of voluntary ankle movements. H-reflex was used for estimating of motoneuron pool excitability. Excitability of the Ia inhibitory pathway was evaluated as a depression of H-reflex by conditioning stimuli of the low threshold afferents in the common peroneal nerve. Movement tasks were controlled by a visually guided tracking method. Major findings were as follows.
1) On ankle dorsiflexion movement reciprocal inhibition of the soleus muscle was recruited in two phases. The first inhibition appeared almost simultaneously with the voluntary agonist EMG.After a recovery from it, the second inhibition developed 100 ms after EMG onset. It was discussed that the 1st and 2nd inhibitions were generated, respectively, by the direct descending command to the Ia inhibitory interneurons and the combined effect on them from descending and delayd agonist Ia inflows via a gamma-loop.
2) Marked disorders in recruitment of reciprocal inhibition were observed in spastic patients with spinal lesions ; i.e., decrease in both the 1st and 2nd inhibitions, an exaggerated recovery into facilitation in-between and finally a reduction in Ia inhibitory activity. The depressed reciprocal inhibitory activity was discussed to be an important factor for motor sidorders in spasticity.
3) On plantar flexion in healthy controls, while facilitation of the agonist soleus H-reflex started several tens ms prior to the voluntary soleus EMG onset and kept increasing after the EMG onset, the Ia inhibition from ankle flexors to extensors was depressed around the voluntary soleus EMG onset. We discussed that this depression of the Ia inhibitory pathway was caused by an increased activity of the extensor counterpart.
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