Short intracortical and surround inhibition are selectively reduced during movement initiation in focal hand dystonia.

Short intracortical and surround inhibition are selectively reduced during movement initiation in focal hand dystonia.
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DOI:
10.1523/jneurosci.3564-08.2008
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发表时间:
2008-10-08
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Hallett M
Hallett M
中科院分区:
其他
文献类型:
--
作者:
Beck S;Richardson SP;Shamim EA;Dang N;Schubert M;Hallett M

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In patients with focal hand dystonia (FHD), pathological overflow activation occurs in muscles not involved in the movement. Short intracortical inhibition (SICI) has been shown to contribute to shaping the output of primary motor cortex (M1) and to be deficient in FHD. Surround inhibition is a neural mechanism which can sharpen desired movement by inhibiting unwanted movement in adjacent muscles. To establish further the phenomenon of surround inhibition and to determine whether SICI might play a role in its genesis, single and paired pulse transcranial magnetic stimulation (TMS), and H-reflex testing were applied to evaluate the excitability of the relaxed abductor pollicis brevis muscle (APB) at various intervals during a movement of the index finger in sixteen patients with FHD and twenty age-matched healthy subjects. While control subjects showed significant inhibition of APB motor evoked potential (MEP) size during movement initiation and facilitation of APB MEP size during the maintenance phase, FHD patients did not modulate APB MEP size. In contrast, SICI was not modulated in any phase in controls, but FHD patients showed reduced SICI during movement initiation. Hmax/Mmax-ratio in control subjects increased only during movement initiation. The results provide further evidence for the presence of surround inhibition in M1, where it occurs only during movement initiation, indicating that different mechanisms underlie movement initiation and maintenance. Thus, surround inhibition is sculpted both in time and space and may be an important neural mechanism during movement initiation to counteract increased spinal excitability. SICI may contribute to its generation, since in patients with FHD, the lack of depression of APB MEP size is accompanied by a reduction in SICI.