Startle decreases reaction time to active inhibition

Exp Brain Res

RESEARCH ARTICLE

Startle decreases reaction time to active inhibition

Anthony N. Carlsen · Quincy J. Almeida · Ian M. Franks

Received: 8 March 2011 / Accepted: 21 November 2011© Springer-Verlag 2011

Abstract In reaction time (RT) tasks where fast ballisticmovements are required, the requisite action is generallypreplanned to enable the quickest responses. When a loudacoustic stimulus (e.g., >120 dB) that elicits a startleresponse is presented during the preplanning phase, themovement is triggered involuntarily and at a suYcientlyshort enough latency to discount normal cortical initiationprocesses. It has been suggested that the startle triggers theaction by providing suYcient additional activation to sur-pass the initiation threshold. It is unclear, however, whethersimilar RT shortening due to startle would occur in theabsence of an excitatory motor output. Thus, in the currentstudy, participants performed a Xexion force oVset (i.e.,inhibition) task within a simple RT paradigm. A startlingacoustic stimulus (SAS) was presented in place of the usual“go” signal on several trials. Results from startle trialsshowed that the inhibitory command could be elicited sub-stantially earlier by an SAS (latency of »78 ms) comparedto control trials (120 ms). This suggests active inhibition ispreprogrammed and can be triggered early by startle in sim-ilar way to traditional “excitatory” tasks. Additionally,early startle-related EMG activity superimposed with thetriggered oVset suggests that the nature of the inhibitory

command used in the current experiment involves theactive suppression of ongoing motor output.

Keywords Inhibition · Startle · Reaction time · EMG · OVset

Introduction

Several recent studies have shown that in humans, deliver-ing a loud acoustic stimulus that elicits a startle reaction canshorten reaction time (RT) for preplanned targeted ballisticmovements (Carlsen et al. 2004b, 2007, 2009; Valls-Soléet al. 1995, 1999). This pattern of results has been repli-cated with diVerent eVectors and movement types includingwrist Xexion (Carlsen et al. 2004b), stepping (Reynolds andDay 2007), saccadic eye movements (Castellote et al.2007), head turning (Siegmund et al. 2001) and anticipatorypostural adjustments (MacKinnon et al. 2007; Siegmundet al. 2001). However, the neural mechanism underlyingthis RT shortening is currently not well understood. Thetypical Wnding from these “startle” experiments is that pre-motor RT (i.e., the time from the stimulus to the onset ofresponse-related muscle activity) is decreased by a largeamount when a startling acoustic stimulus (SAS) unexpect-edly replaces the normal imperative “go” signal (for areview see Carlsen et al. in press). For example, when a 124dB acoustic stimulus was presented in a simple RT taskwhere the wrist extension movement could be preplanned,mean premotor RT was decreased from 142 ms to 85 mswith several observed RTs of 55–65 ms (Carlsen et al.2004b). Importantly, it was the absolute value to which RTwas decreased that was of particular note rather than therelative magnitude of the RT shortening. Since several ofthe observed RTs following the SAS were <65 ms, it was

A. N. Carlsen (&)School of Human Kinetics, University Ottawa, 325-125 University Private, K1N 6N5 Ottawa, ON, Canadae-mail: [email protected]

Q. J. AlmeidaSun Life Financial Movement Disorders Research and Rehabilitation Centre, Wilfrid Laurier University, Waterloo, ON, Canada

I. M. FranksSchool of Kinesiology, University British Columbia, Vancouver, BC, Canada

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argued that the initiation of the movements could not havebeen mediated by the typical cortical information process-ing circuits (Carlsen et al. 2007, 2009; Rothwell 2006;Valls-Solé et al. 1999, 2008). Thus, it appeared that the pre-pared movement was not “voluntarily” initiated at a shortlatency but rather was involuntarily triggered when theSAS evoked a startle reaction. This implies that the prepro-grammed motor plan was triggered at short latency viainteractions between lower-level (i.e., subcortical) startle-related pathways and higher-level voluntary response path-ways (Rothwell et al. 2002; Rothwell 2006).

A recent model of motor preparation and initiation sug-gests that the startle triggers the action by providing suY-cient additional cortical activation via a fast, subcorticallymediated ascending pathway to surpass the initiationthreshold for the planned movement (Carlsen et al. inpress). However, it is unclear whether planning an actionthat would result in suppression of motor output at themotor neuron pool would be susceptible to similar RTshortening. While startle facilitation of inhibitory posturaladjustments has been previously shown (MacKinnon et al.2007; Valls-Solé et al. 1999), these have always been in thecontext of an “active excitatory” movement such as step-ping or rising onto the toes.

For more traditional movement tasks involving the activeonset of a muscle, preparation is evidenced by a slowlyincreasing potential measured at the scalp. This activity beginsup to 1.5 s prior to the movement onset and is thought to reXectpremovement preparatory cortical activity (Cui et al. 1999; Cuiand MacKinnon 2009; Deecke et al. 1976; Kornhuber andDeecke 1965). Interestingly, cortical preparatory activity spe-ciWcally related to voluntary oVset has been shown previouslyusing a movement-related potential (MRP) measured usingEEG. This MRP preceding voluntary relaxation has been dem-onstrated in a unidirectional force oVset task (see Terada et al.1995). Rothwell et al. (1998) also reported the existence of acortical MRP preceding the oVset of an isometric pinch task(e.g., bidirectional force oVset), although the MRP was signiW-cantly smaller than the MRP seen in voluntary activation tasks.The diVerence in oVset MRP amplitude between these twoexperiments was attributed to the diYculty, and hence, mode ofinhibition used in the respective tasks. In particular, it was sug-gested that a pinch oVset was a relatively easy oVset task as itsimply required the withdrawal of ongoing cortical drive toboth the agonists and antagonists (Rothwell et al. 1998). Incontrast, it was suggested that the isotonic oVset task used byTerada et al. (1995) was more diYcult and resulted in a largerMRP due to the requirement to preplan the “active inhibition”of lower centers in order to avoid unwanted associated volun-tary activity in the antagonist muscle (Rothwell et al. 1998).

It was of interest whether a startle could trigger a focalinhibitory action since the planned output would result in adecrease in motor output rather than an increase. In order to

test this possibility, the current experiment employed a vol-untary “oVset” task where the primary goal was to inhibit(or stop) ongoing force production (and EMG activity)when a signal was given. The speciWc aim of this experi-ment was to determine whether the RT decrease observeddue to startle could occur independently of a descendingcommand related to active excitation. This was examinedby investigating the eVect of an SAS on the performance ofa simple RT task involving the oVset of muscle activity inthe arm. It was hypothesized that the presentation of anSAS would result in the RT shortening for the voluntaryinhibition task that was similar to that seen for excitatoryvoluntary movement tasks used previously.

Experimental procedures

Participants

Ten participants (4 men, 6 women; age 22 § 5 years) withno obvious upper body abnormalities, or sensory or motordysfunctions volunteered to participate in the study. Allparticipants gave written informed consent. The study wasconducted in accordance with the ethical guidelines set byWilfrid Laurier University and conformed to the Declara-tion of Helsinki.

Apparatus and task

Participants sat with the right forearm secured in a pronatedposition with the palm down, to a custom-made aluminummanipulandum that moved in the horizontal plane with anaxis of rotation about the elbow (Fig. 1). The home position(90° of Xexion at the elbow with the shoulder Xexed andabducted 30°) was indicated by a physical stop. Participantsperformed a force oVset task, where they were told to “getready” by Xexing the elbow to create a targeted force valueagainst the physical stop, and to release the force withoutany overt arm extension activity as quickly as possible fol-lowing the onset of an acoustic “go” stimulus. A voluntarytask involving the release of a Xexion force was chosenbecause the generalized motor response observed followinga startling acoustic stimulus is predominantly one of Xexion(Landis et al. 1939). Thus, in this “oVset” task, a voluntaryinhibition of Xexion was chosen in opposition to the reXex-ive Xexion activation.

Real-time position feedback was provided during trialswith a 1-cm-wide yellow horizontal line on a computerscreen whose vertical movement within a 15-cm-tall £1-cm-wide box corresponded directly to the force generatedagainst the physical stop (approximately linear at 0.25 cm/N).The starting (home) position for the marker was at the bot-tom end of the box (see Fig. 1). The target was represented

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with a similar 1-cm-wide marker line (blue), located 10 cmvertical to the start position and represented 40 N force.This was chosen because it represented a moderate level offorce and resulted in consistent EMG production acrosssubjects without causing excessive fatigue. After each trial,RT feedback (ms) was displayed on the screen. Participantswere allowed to freely assess how their force productionaVected the feedback prior to testing to become familiarwith the task and equipment. Prior to performing the task,participants received a single block of 10 practice trials.

Instrumentation and stimuli

Each trial started with a visual “get ready” warning signalin addition to a short acoustic warning tone (100 ms,300 Hz, 80 dB). Participants initiated a right elbow Xexionto generate a 40 N force (20 Nm torque) after the warningtone. Once the force level was reached, a random forepe-riod of 2–3 s was initiated. Following the foreperiod, acomputer program generated the imperative “go” stimulusconsisting of a narrow band noise pulse (1 kHz, 40-msduration) that was ampliWed and presented via a loud-speaker (M58H, MG Electronics) placed directly behindthe head of the participant with an intensity of either 82 dB(control) or 124 dB (startle) SPL measured using the “A”weighted scale at a distance of 30 cm from the loudspeaker

(approximately the distance to the ears of the participant).Prior to testing, participants were instructed that the loud-ness of the stimulus would be variable.

Each participant performed 32 trials, comprised of 28control trials with 4 startle trials pseudorandomly dispersedamong the control trials (with the stipulation that no 2 con-secutive trials were startle trials, and no startles occurredwithin the Wrst 3 trials). The approximate trial-to-trial inter-val was 10 s, although this varied due to the random forepe-riod (see above).

Surface EMG data were collected from the right elbowprime movers: the long head of the biceps brachii (BIC)and the lateral head of triceps brachii (TRI), as well as fromthe startle response indicator sternocleidomastoid (SCM)using bipolar preampliWed surface electrodes connected viashielded cabling to an external ampliWer system (modelAMT-8, Bortec Biomedical). Force was monitored using athin Wlm force transducer (FlexiForce A201, Tekscan Inc.)attached to the physical stop for the manipulandum. Datawere sampled at 1,000 Hz (National Instruments PCI-6024E) for 1.5 s, beginning 500 ms prior to the “go” signal,using a customized program written with LabVIEW® soft-ware (National Instruments Inc.).

Data reduction and analysis

Premotor RT was the chosen measure of RT for the currentstudy as it represents an estimate of the total central pro-cessing time and was deWned as the time from the “go” sig-nal until an oVset of ongoing EMG activity in the bicepsmuscle. Surface EMG oVsets were determined by Wrst dis-playing the EMG pattern on a computer monitor with asuperimposed line, indicating the point at which the EMGactivity (calculated from EMG rectiWed and Wltered with a25-Hz low-pass elliptic Wlter) decreased more than 2 stan-dard deviations (SD) below baseline (mean of 100 ms ofEMG activity preceding the “go” signal). OVset was thenveriWed by visually locating and manually adjusting theoVset mark to the point at which the activity Wrst started todecrease on the raw EMG trace. This method allows forcorrection of errors due to the strictness of the algorithm.During initial analysis, there appeared to be additionalEMG activation superimposed with the BIC activity thatwas transiently interrupted by the oVset on startle trials (seeFig. 2 startle, for example data). In order to attempt toquantify this observation, a secondary analysis was per-formed where the duration of the BIC silence was calcu-lated, and integrated EMG (iEMG) values were computedfor each trial. Raw rectiWed EMG was numerically inte-grated for 50 ms (ms time base) immediately prior to themarked oVset of BIC and for 50 ms immediately precedingstimulus onset to assess the apparent observed increase inEMG activity just prior to oVset in startle trials. All startle

Fig. 1 Overhead view of participant position and a depiction of theexperimental task. An elbow Xexion was made against a physical stopto produce a force of 40 N upon the “get ready” signal, and the forcewas released upon the “go” signal. Visual feedback of force generatedwas represented by a cursor, and a target represented the 40 N targetforce. A loudspeaker placed behind the participant delivered the “go”and startle stimuli. See text for further details

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trials were included, and 5 randomly selected control trialswere used from each participant in order to more closelymatch the number of trials included in the average. Addi-tionally, for the startle trials, the duration of silence in BICwas assessed by placing a new marker at the point at whichEMG activity increased more than 2 SD above the silence.The diVerence between the oVset and onset time points wascalculated as the BIC silence duration.

Errors were recorded when any overt EMG burst in TRI(at least 25 ms of activity 2 SD above baseline) wasdeemed to be responsible for the initial release of force byappearing prior to any BIC oVset. These trials were dis-carded from analysis. This was done so that “voluntary”BIC oVset trials could be examined rather than BIC oVsetsthat were associated with voluntary extension-related acti-vation in TRI (e.g., reciprocal inhibition). If more than 2(>50%) startle trials or more than nine (>32%) control trialswere discarded for any single participant, data from thatparticipant were excluded from EMG analysis of the oVsettask. This procedure led to data being excluded from 3 ofthe original 10 participants.

Statistical analyses

Dependent variables were analyzed using repeated mea-sures ANOVA procedures described below. Prior to analy-sis, proportion variables were subjected to an arcsine square

root transform. Greenhouse–Geisser corrected degrees offreedom were used to correct for violations of the assump-tion of sphericity. DiVerences with a probability of less than.05 were considered to be signiWcant. Tukey’s honestly sig-niWcant diVerences (HSD) post hoc tests were administeredwhere necessary to determine the locus of any diVerences.

Results

Error rate

As previously mentioned, three participants were unable toconsistently perform the required oVset task, since exten-sion EMG activity in TRI associated with the initial releaseof force was detected following the “go” signal in a largeproportion of trials. These three data sets were removed asdescribed above. For the remaining seven participants,there was no signiWcant diVerence in error rate betweencontrol (6%) and SAS trials (14%), P = .513, leaving a totalof 24 SAS trials in the oVset task to analyze. Thus, althoughcare should be exercised in the interpretation of theseresults due to the small number of trials, in many cases thedata from these few trials nevertheless led to statisticallystrong signiWcant diVerences.

OVset

Premotor RT (time to oVset) was analyzed using a one-way(control 82 dB vs. startle 124 dB) repeated measuresANOVA. A signiWcant main eVect was found for stimulus,F(1,6) = 40.577, P = .001, �p

2 =.871, indicating that pre-motor RT (time to EMG oVset) was shorter (77.8 § 8.6 ms)when the startling acoustic stimulus (SAS) accompaniedthe “go” signal compared to control (119.9 § 14.7 ms). Asnoted above, the duration of BIC silence in startle trails wascalculated; however, only descriptive statistics are avail-able: Mean BIC silence duration was found to be 115.9 mswith a mean within-subject standard deviation of 25.8 ms.

EMG amplitude

In order to determine whether the startle interacted with thevoluntary response, EMG amplitude was comparedbetween control and startle trials. A 2 (stimulus) £ 2 (time)repeated measures ANOVA was used to compare theamount of EMG activity recorded (i.e., iEMG area) in a50-ms window immediately prior to BIC oVset with EMGactivity just prior to the “go” signal in both SAS and controltrials (see Fig. 3a—gray areas). Mean iEMG data areshown in Fig. 3b. Main eVects for both time and stimuluswere observed and superseded by a signiWcant interactioneVect, F(1,6) = 7.075, P = .038, �p

2 =.541. Post hoc analysis

Fig. 2 Example raw EMG (black) and force (gray) from a single con-trol trial (top) and a single startle trial (bottom). Time zero is the timeof the “go” signal or SAS. Note that in the startle trial, the much shorterlatency to oVset compared to control, and the increase in EMG activityjust prior to oVset at 93 ms. Secondly, note the resumption of startle-related activity approximately 130 ms later

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showed that in the 50 ms leading up to BIC oVset, there wassigniWcantly more EMG activity in startle trials comparedto control (P < .01). Importantly, no signiWcant diVerencesin the amount of EMG activity were apparent between con-trol and startle trials for the 50-ms period immediately priorto the stimulus, or between the two time points in controltrials (P > .05).

Discussion

In previous studies, it has been shown that a prepro-grammed motor response was produced at a much shorter

latency when an SAS was presented in place of the regular“go” signal in RT tasks (Carlsen et al. 2004a; Valls-Soléet al. 1999). While the voluntary response was elicited witha latency normally associated with a startle reaction (e.g.,<70 ms), the EMG timing characteristics were unchanged,suggesting that the voluntary response was not simplyadded on to the early startle reXex, but involuntarily trig-gered by the startle response activation (for reviews see,Carlsen et al. in press; Valls-Solé et al. 2008). Although theprecise mechanism of this triggering is a matter of debate, ithas recently been suggested that the neural activation pro-vided by the startle reXex via an ascending pathway pro-vides suYcient additional activation to a cortically preparedresponse to irreversibly initiate the entire action (Carlsenet al. in press). However, this model relies on the notionthat action preparation can be viewed as the increased acti-vation of a group of cortical neurons representing a motorprogram, known as a “cell assembly” (see Hebb 1949;Wickens et al. 1994), to a level just below an initiationthreshold. It was of interest whether similar processes wereinvolved in a task that resulted in suppression of motoroutput at the motor neuron pool.

The aim of the current experiment was to determinewhether presenting a startling acoustic stimulus (SAS) in anRT task involving voluntary inhibition of ongoing muscleactivity would result in RT shortening similar to that seenpreviously in RT tasks involving the initiation of an excit-atory contraction. When an SAS was presented in an RTtask requiring the stopping of force production through thevoluntary oVset of ongoing muscle activity, RTs for this“oVset” task were substantially shortened from 120 ms incontrol trials to 78 ms. Since the startle RT eVect observedwas similar to that previously observed for voluntary onsetRT tasks (i.e., those requiring activation and contraction ofa muscle to achieve the movement goal), these results sug-gest that the processes mediating the preparation and initia-tion of both “active excitatory” and “active inhibitory”motor tasks are similar.

Previous studies that have used a force oVset task aresimilar to the one used in the present experiment (seeTerada et al. 1995). It was suggested that “active inhibi-tion” was used to perform this type of task so that unwantedassociated voluntary activity in the antagonist musclewould also be suppressed (Rothwell et al. 1998). Indeed, inthe current experiment, many participants found therequirement of performing the oVset while avoiding activa-tion of the antagonist particularly challenging, even follow-ing practice. This led to the elimination of data from threeparticipants due to their inability to consistently performthe biceps Xexion oVset without overt triceps extensionEMG activity. Therefore, we assert the task used here likelyinvolved the planning of active inhibitory control ratherthan simply the withdrawal of ongoing activity. This active

Fig. 3 EMG activity in the oVset task for both the control and startleconditions. Top panel a shows ensemble averaged rectiWed EMGactivity across participants aligned to time of marked EMG oVset (time0) for both the startle and control conditions. Gray sections representtime windows where integrated EMG (iEMG, see text) was calculated,and vertical dashed lines represent mean time onset of imperative “go”signal with respect to BIC oVset. Bottom Panel b shows mean (§SE)iEMG for control (black) and startle (white) trials calculated in 50-mstime windows starting 50 ms prior to “go” (‘go’-50) and 50 ms prior tomarked biceps oVset (BIC oVset-50). *=P < 0.01

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inhibition may have acted either at a cortical level, subcor-tical level, spinal level, or all three.

Several lines of evidence support the suggestion thatthe type of oVset task used here involved the preplanningof active inhibition in inhibitory cortical motor circuits.The excitability of intracortical inhibitory GABAergiccircuits in motor cortex can be assessed using paired-pulse transcranial magnetic stimulation (TMS) with ashort (e.g., 2.5 ms) inter-stimulus interval (Di Lazzaroet al. 1998; Kujirai et al. 1993; Rothwell et al. 2009). Inthis method, termed short latency intracortical inhibition(SICI), a Wrst subthreshold TMS pulse, is used to condi-tion the eVect of a second suprathreshold TMS pulse. TheWrst pulse activates low threshold inhibitory circuits,whereby the amplitude of the motor evoked potential(MEP) caused by the second pulse depends on preexistinginhibitory circuit excitability (Rothwell et al. 2009).Buccolieri et al. (2004) applied paired-pulse TMS overthe hand area of primary motor cortex, while participantsperformed an RT task requiring the relaxation of indexWnger abduction. Results showed that SICI was increased30 ms prior to this type of active inhibition oVset task.This suggests that for the task used by Buccolieri et al.(2004), as well as the similar task used in the currentexperiment, increased activation of GABAergic corticalinhibitory circuits plays a critical role in actively decreas-ing neural activity at a cortical level related to the ongoingproduction of force. Furthermore, since we show here thatthis type of oVset task can be speeded by startle in thesame way as an active onset, it appears that active inhibi-tory circuits can also be preprogrammed and thus mayinvolve increased neural activation in cell assemblies in away similar to that described for excitatory tasks. In bothactive excitatory and active inhibitory tasks, it appearsthat the startle can act to provide the prepared motor pro-gram suYcient activation via ascending reticulo-thalamo-cortical pathways (see Carlsen et al. in press) to overcomeinitiation threshold, resulting in the early, involuntarytriggering of the motor program without the usual corticalcommand.

It is thus far unclear whether the observed active inhi-bition triggered by the SAS has an eVect primarily at thecortical level, resulting in the cessation of excitatory driveto the motor neuron pool, or whether inhibitory descend-ing commands also suppress the motor neuron pooldirectly. Some initial evidence for direct suppression oflower centers such as spinal motor neuron pools may beprovided by the inXuence of the active inhibitory com-mand on the descending startle response volley. The star-tle response itself does not require cortical loops andprimarily consists of projections directly from the pontinereticular formation to various levels of the spinal cord(Yeomans and Frankland 1996). If the active inhibitory

command simply resulted in withdrawal of voluntarydescending excitatory activation, there should be no eVecton the startle-related activation. Unfettered, the startleresponse in ECR is continuous for 100–200 ms (Brownet al. 1991). However, the startle response that was elic-ited was largely attenuated in the target muscle for a brieftime (Fig. 3a). There are two possible explanations forthis observation: First, it may be that the voluntary oVsetcommand in the task used here involved descendinginhibitory signals that decreased the excitability of themotor neuron pool at a spinal level suYciently to alsosuppress the descending startle-related EMG activationfor a brief amount of time until the activation level associ-ated with a relaxed state stabilized. This explanationwould be in line with that of Rothwell et al. (1998) whosuggested that this type of oVset task might require thedirect suppression of spinal motor centers. Alternatively,it is possible that the active inhibitory command aVectedthe startle response by acting to inhibit subcortical motorstructures that are also related to the startle response suchas the pontine reticular formation (Yeomans and Frank-land 1996). This would have also resulted in the cessationof excitatory descending startle response activity. While itis unclear whether the voluntary oVset command and thereXexive startle response converged at the muscle level,motor neuron pool, or brainstem level, the startle responsewas suppressed by the descending “oVset” command for ashort time before being expressed once again (Figs. 2 and3a). While this experiment was not designed to directlymeasure this variable, the data here suggest that the dura-tion of this inhibitory command is approximately 116 ms.Further study may clarify this result.

Interestingly, while analyzing the data and viewing rawEMG traces, there often appeared to be an increase inbiceps EMG activity preceding the voluntary oVset in manytrials where an SAS was presented. Several previous stud-ies that have presented an SAS in the context of an RT taskhave shown that while the movement produced at shortlatency following an SAS was largely unaVected (in termsof kinematics and EMG timing), the amplitude of the WrstEMG burst related to the required movement was larger instartle trials than control trials (Carlsen et al. 2003, 2004b;Kumru and Valls-Solé 2006; Siegmund et al. 2001). It wassuggested that this increased amplitude may be the result ofthe startle volley interacting and summing with the speededdescending voluntary command, particularly in more proxi-mal muscles (Carlsen et al. 2004b; Siegmund et al. 2001,2008). A simple summation model presented by Siegmundet al. (2008) suggested that this startle-related EMG activityembedded within the voluntary response EMG may play arole in the shortening eVect of startle on RT. SpeciWcally,startle-response-related neural activity arriving shortlyprior to the voluntary response activity may drive the motor

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neuron pool toward threshold, allowing for an overtresponse to be expressed slightly earlier than by the voluntaryactivation alone. However, it is diYcult to observe and dis-entangle superimposed voluntary and reXexive activationresponses when they occur at the same time (i.e., they arefully superimposed).

Some evidence for superimposed startle-related activitywas observed in the current study, whereby it appears thatthe startle activity arrived slightly in advance of the volun-tary oVset response. In particular, in startle trials, there wasan increase in iEMG activity in the 50 ms immediately pre-ceding the voluntary oVset compared to baseline (Figs. 2and 3). Although it may appear small, this (almost twofold)increase in activation can only be attributed to the presenta-tion of an SAS and thus a startle response, since it was notobserved in control trials. This activation suggests that thestartle response is indeed superimposed on the SAS-elicitedearly voluntary response and that in the case of the oVsetmovement preceded the marked oVset by several millisec-onds (Fig. 3). It is diYcult to quantify the latency of thevoluntary oVset response with respect to the startleresponse onset on a trial-to-trial basis since the amplitude isrelatively small and may only be evident once several trialsare averaged together. That said, it is clear that some (pre-sumably) startle-related EMG activity precedes the volun-tary oVset in SAS trials, and future experiments designed toinvestigate this may be able to more accurately quantify thetiming.

Conclusions

In summary, the present experiment investigated the eVectof an SAS on the performance of a simple RT paradigminvolving a force oVset task. Results from startle trialsclearly showed that for a focal oVset task, the command ispreprogrammed and can be elicited early (premotor RTlatency of »78 ms) by an SAS. This suggests that prepara-tory processes and structures mediating an oVset task aresimilar to those used in traditional excitatory tasks. Itappears however that some summation of the startleresponse with the initial EMG activity is present. This wasmost clearly shown whereby a small amount of startle-related EMG activity was observed occurring slightly inadvance of the voluntary oVset in the force release task.Since the voluntary command also resulted in suppressionof the startle response, it appears that the oVset taskemployed active inhibition of subcortical and/or spinalstructures.

Acknowledgments This research was supported by grants from theNatural Sciences and Engineering Research Council of Canada(NSERC) awarded to IM Franks and to QJ Almeida.

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