The early release of planned movement by acoustic startle can be delayed by transcranial magnetic stimulation over the motor cortex
Non‐technical summary Reaction times of planned movements can be reduced to less than 100 ms when a startling acoustic stimulus (SAS) is presented immediately prior to, or coincident with, the imperative ‘go’ cue. Based on the short latency of these reaction times, it has been suggested that the ea...
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Published in | The Journal of physiology Vol. 590; no. 4; pp. 919 - 936 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.02.2012
Wiley Subscription Services, Inc Blackwell Science Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Non‐technical summary Reaction times of planned movements can be reduced to less than 100 ms when a startling acoustic stimulus (SAS) is presented immediately prior to, or coincident with, the imperative ‘go’ cue. Based on the short latency of these reaction times, it has been suggested that the early release of planned movements by a SAS is mediated by shorter pathways that pass through the brainstem instead of via the primary motor cortex. Here we show that the application of high intensity transcranial magnetic stimulation over the primary motor cortex, a method that suppresses the excitability of the motor cortex and blocks voluntary drive, caused a significant delay in the onset of SAS‐released movements. These findings provide evidence that the early release of planned movements by a SAS is mediated, in part, by pathways that pass through the primary motor cortex.
Previous studies have shown that preplanned movements can be rapidly released when a startling acoustic stimulus (SAS) is presented immediately prior to, or coincident with, the imperative signal to initiate movement. Based on the short latency of the onset of muscle activity (typically in less than 90 ms) and the frequent co‐expression of startle responses in the neck and eye muscles, it has been proposed that the release of planned movements by a SAS is mediated by subcortical, possibly brainstem, pathways. However, a role for cortical structures in mediating these responses cannot be ruled out based on timing arguments alone. We examined the role of the cortex in the mediation of these responses by testing if a suprathreshold transcranial magnetic stimulation applied over the primary motor cortex, which suppresses voluntary drive and is known to delay movement initiation, could delay the release of movement by a SAS. Eight subjects performed an instructed‐delay task requiring them to make a ballistic wrist movement to a target in response to an acoustic tone (control task condition). In a subset of trials subjects received one of the following: (1) suprathreshold TMS over the contralateral primary motor cortex 70 ms prior to their mean response time on control trials (TMSCT), (2) SAS 200 ms prior to the go cue (SAS), (3) suprathreshold TMS 70 ms prior to the mean SAS‐evoked response time (TMSSAS), or (4) TMSSAS and SAS presented concurrently (TMS+SAS). Movement kinematics and EMG from the wrist extensors and flexors and sternocleidomastoid muscles were recorded. The application of TMSCT prior to control voluntary movements produced a significant delay in movement onset times (P < 0.001) (average delay = 37.7 ± 12.8 ms). The presentation of a SAS alone at −200 ms resulted in the release of the planned movement an average of 71.7 ± 2.7 ms after the startling stimulus. The early release of movement by a SAS was significantly delayed (P < 0.001, average delay = 35.0 ± 12.9 ms) when TMSSAS and SAS were presented concurrently. This delay could not be explained by a prolonged suppression of motor unit activity at the spinal level. These findings provide evidence that the release of targeted ballistic wrist movements by SAS is mediated, in part, by a fast conducting transcortical pathway via the primary motor cortex. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 |
ISSN: | 0022-3751 1469-7793 1469-7793 |
DOI: | 10.1113/jphysiol.2011.219592 |