ELECTROPHYSIOLOGICAL CORRELATES OF BEAT INDUCTION AS

INTERNALLY- AND EXTERNALLY-GUIDED ACTION

1
Neil P. Todd and
2
Ellen Seiss
1
Department of Psychology, University of Manchester, M13 9PL, UK.
2
Behavioural and Brain Sciences Centre, University of Birmingham, B15 2TT, UK.
ABSTRACT
In this paper we report the results of an ERP experiment (64-
channel EEG) to investigate brain processes underlying beat
induction. Musically trained subjects were required to listen to an
anapest rhythm, consisting of three clicks, with inter-onset
intervals of 500 ms, and a gap of 1000 ms, under active and
passive conditions, preceded by a condition in which the stimulus
was unpredictable. A further condition was added which
introduced uncertainty into the presence or absence of the third
click. The results show that the evoked N2 is enhanced in regular
as compared with random stimuli. Random omission of the third
click on 50% of trials suppresses the N2 in the third interval but
induces a later N3 when the 3
rd
click is present. Comparing active
and passive conditions indicates that pre-movement negativities
(PMN) overlap spatiotemporally with the regular N2 consistent
with the N2 including a component which may be a correlate of
movement preparation. We interpret the potentials as being
consistent with the operation of two distinct sensorimotor circuits:
(1) an automatic, internally driven circuit involving SMA for
which the N2 may be a manifestation, and (2) an attention
dependent, externally driven circuit involving PPC for which the
N3 may be a manifestation. Likely both circuits are co-activated
during the presentation of a rhythmic stimulus but the relative role
of the two will depend on the predictability of the rhythm.
1. INTRODUCTION
Beat induction or pulse sensation refers to the phenomenon
whereby a metrical rhythm gives rise to a sense of isochronous
pulse or beat (also known as the tactus). Research on beat
induction overlaps with the field of sensorimotor synchronisation
in which the principal experimental paradigm is synchronisation
of simple repetitive movements with metronomic stimuli.
Experimental studies of beat induction thus have similar
methodologies, e.g. tapping, except that they involve non-
isochronic, metrical rhythms as stimuli with a particular focus in
the induction of a regular down beat, including in intervals for
which there is no explicit stimulus present. Thus beat induction
may be thought of as a kind of "mental continuation". Of
particular relevance to this study is the established fact that beat
induction has an existence region, i.e. the sense of pulse only
occurs for metrical rhythms with a range of beat interval between
about 300 and 900 ms with median about 450 ms (Moelents and
van Noorden, 1999) which las led some authors to draw a parallel
with natural rates of locomotion. The sense of pulse is also
enhanced by syncopation, i.e. when rhythmic events do not fall on
a predicted down beat.
Whilst there are now numerous computational models and
algorithms which attempt to simulate beat finding (for review see
Todd , OBoyle and Lee, 2002) there are essentially only two
theories which give an account of beat induction which have a
bearing on possible underlying brain mechanisms in humans: (1) a
beat is an attentional oscillation (AO) (Large and Jones, 1999)
and (2) a beat is a movement intention (MI) (Todd et al., 2002).
The AO theory supposes that there exists in the brain a network of
coupled oscillators which synchronise with a periodic stimulus.
The MI theory in contrast supposes that beat induction is a form of
sensoriguided action in which the well-established motion
planning network, involving pre-motor cortex (PMC), posterior
parietal cortex (PPC) and cerebellum, is activated in conjunction
with temporal coding of stimulus properties in auditory cortex by
means of the modulation power spectrum.
In this study we seek to investigate brain processes underlying
beat induction by means of high resolution (64-channel) EEG. In
particular we seek to find neurophysiological correlates of motion
planning in a passive listening task in order to provide evidence
for the MI theory. ERPs are an excellent tool for investigating
sensorimotor synchronisation, given the fine temporal resolution,
and produce well-defined stimulus and movement related
potentials. Whilst MEG has advantages in some circumstances
and has been used to identify stimulus and movement related brain
events (Muller et al., 2000) for sensorimotor synchronisation
MEG is less suitable for longer latency N2/P3 waves which are of
interest in cognitive planning. A recent study of error correction in
sensorimotor synchronisation by Praamstra et al. (2003) using
EEG gives examples of stimulus and movement related potentials
which are of relevance here and which we use as a basis for the
identification of the various components in our study. Essentially
there are three morphologies: (a) stimulus related potentials
(SRPs), consisting of a P1, N1, P2 and N2, (b) movement related
potentials (MRPs), consisting of a PMN, a re-afferance negativity
(RAN) and a post-motion positivity (PMP) and (c) a hybrid
SRP/MRPmorphology, obtained by locking the averaging to the
stimulus during active synchronisation.
The aim of the study reported here was to use a modification of
the standard procedure for sensorimotor synchronization by
stimulating with an anapest rhythm, rather than an isochronous
sequence, consisting of three clicks and a gap in which a target
beat is induced. The idea being that the gap would allow
investigation of brain activity, either passive or active, induced
before, at and after the target without being immediately masked
by the standard SRPs. We hypothesized that potentials in the gap
should show evidence of movement relatedness even in a passive
condition.
ISBN 1-876346-50-7 2004 ICMPC 212


2. METHOD
Subjects
10 musically trained subjects were selected from staff and
students at the University of Birmingham. Subjects were all right
handed and had no hearing or cognitive impairments.
Stimuli
Stimuli were 1 ms, compressive square pulses, producing a robust
click, presented at a loud but not uncomfortable intensity.
Apparatus
EEG, EMG and EOG were recorded continuously with Ag/AgCl
electrodes located in scalp, muscle and periocular positions.
Finger movements were recorded using a force-plate transducer.
EEG locations were given by the 10-5 extension of the 10-20
system. EMG was recorded differentially in positions above the
flexor and extensor indicies muscles. All signals were amplified
by BioSemi Active-One Amplifiers and sampled at 512 Hz.
Stimuli generated using Eprime software and delivered by
detachable headphones placed under the cap.
Procedure
After preparation subjects were seated in a comfortable chair and
were given instructions. They were told that they would be
presented with a number of rhythms in sessions lasting about 4
mins. At the start of each session they would be given a warning
tone. During the sessions they were to be as relaxed as possible
and avoid unnecessary movements with gaze fixated but to
maintain attention on the rhythm. Recordings were made under
four conditions consisting each of two blocs of about 4 mins.
The first three conditions were passive. The first was a random
condition (300 repetitions), in which the inter-onset interval of the
clicks varied randomly between 1000 and 2000 ms with a
rectangular probability distribution. The second was a regular
condition (200 repetitions), in which an anapest rhythm was
presented consisting of three clicks with inter-onset interval of
500 ms (close to the optimum interval) followed by a gap of 1000
ms. The third was a regular-uncertain condition (400 repetitions),
in which the anapest rhythm was randomly alternated with a
rhythm consisting of two clicks with inter-onset interval of 500 ms
followed by a gap of 1500 ms. The fourth condition was active
(200 repetitions) in which the subjects were to synchronise
extension of their right index finger to the beat of the regular
anapest rhythm. They were given explicit instructions on what
was meant by the beat, including the missing beat in the gap. They
were also instructed that the required movement was a flick
without any using any force on the return and without movement
of the other fingers. This was to avoid significant activity in the
flexor muscle. The movement target was a tap on the force-plate
which was adjusted to be about 2 cm from the index finger which
at rest hung loosely over the end of the arm rest.
EEG/EMG analysis
EEG was segmented into epochs off-line according to triggers
which were time-locked to the stimuli. Epochs containing
significant artifacts were rejected from the analysis. Averages
were obtained for each of the four conditions for each subject and
grand means obtained for each condition. For the regular uncertain
condition the averaging was carried out separately for those trials
with the 3rd beat present and those with the 3rd beat missing.
EMG was rectified and low-pass filtered and averaged in the same
way. Due to excessive artifact, data from two of the subjects were
not included in the final analysis.
3. RESULTS

Figure 1: Grand mean from 8 subjects for the random condition.
Potentials are centred at FCz with potentials measured at
surrounding electrodes also shown.
Considering first the random condition (Figure 1) N1, P2 and N2
potentials are identifiable with latencies of about 95, 190 and 280
ms and with amplitudes of about -5.0, +6.5 and 1.5 V
respectively at FCz. Source analyses of the N1 supported a
bilateral tangential source from within the sylvian fissure
(Talairach-Tournoux coordinates, X=-48.7, 43.6, Y=-30.9, -30.4,
Z=19.2, 23.1, RV = 2.8%). The N2, which was highly focussed
over FCz, could be explained by a single source in medial frontal
gyrus (BA 6) corresponding to the supplementary motor area
(SMA) (Talairach-Tournoux coordinates, X=+5, Y=-21, Z=62,
RV = 4.8%). A bilateral source model placed the generators near
to the central sulcus and was therefore considered to be
implausible.

Figure 2: Grand mean (centred at FCz) from 8 subjects for the
regular anapest condition.
In the regular anapest condition N1, P2 and N2 potentials can be
also identified for each of the three clicks within the anapest. For
the third interval prior to the gap these have peak latencies of
about 90, 150 and 270 ms with amplitudes of about -0.8, +1.8 and
-2.0 V at FCz. Thus all three waves peak earlier than the random
condition. For amplitude the N1/P2 is significantly reduced in
ICMPC8, Evanston, IL, USA August 3-7, 2004
213


amplitude compared with the random condition and appears to
show adaptation over course of the anapest rhythm so that they are
largest following the gap. The N2 in contrast appears to show
integration over the anapest rhythm so that it is largest prior to the
gap.
Inspection of scalp distribution showed that the later aspect of the
N1, up to about 120 ms, prior to the gap developed a more lateral
distribution. Consistent with previous analyses (Scherg et al.
1989) the distribution could be explained by an additional bilateral
radial source, the N150, superposed with the bilateral tangential
source. The position of the N150 was located in BA 42 near the
lateral surface of the superior temporal gyrus (Talairach-Tournoux
coordinates, X=-65.9,+65.9, Y=-30.2, Z=8.4, RV = 5.8%). The
tangential source was fixed at the position and orientation of the
N1 from the random condition.

Figure 3: Scalp distribution of the N2 for the random case (left)
compared with the N2 prior to the gap in regular anapest (right).
The N2 prior to the gap in contrast to the random N2 was more
widespread (Figure 3), as well as being larger in magnitude, and
hence a bilateral source model seemed more appropriate.
However, this gave coordinates, X=-20,+20, Y=-14.3, Z=43.8,
(RV = 5.3%), which would place the sources at the juncture
between anterior cingulate cortex (BA 24) and medial frontal
gyrus (BA 6), and was therefore ambiguous.
In addition to the potentials which could be compared with the
random condition there was a P3 which followed the N2 prior to
the gap and a series of emitted waves in the gap. The P3 had with
a latency of about 370 ms and could be explained by a bilateral
source within the sylvian fissure in BA 41 but more caudal than
the N1 generators (Talairach-Tournoux coordinates, X=-
39.5,+39.5, Y=-41, Z=10.7, RV = 4.5%). The series of emitted
waves in the gap appeared to be an echo of the evoked
potentials in the 3
rd
interval and hence were labelled eN1, eP2,
eN2 and eP3. The eN1/P2 obtained just after the target beat had
latencies of about 90 and 140 ms with small amplitudes. The
eN2/P3 obtained from the average before the 1st click had
latencies of about 300 and 350 ms with amplitudes of about -1.0
and +0.3 V. Reliable source analyses were not obtainable for the
emitted potentials nor were they readily identifiable in the
individual averages.
Considering now the regular uncertain condition (Figure 4) in the
first two intervals prior to the 3rd beat, the morphology of the
three stimuli are very similar but with two subtle differences. In
both variants of the uncertain condition the size of the P2s were
larger, but the N1s not so, and there was a general enhanced
negativity prior to 3rd beat.

Figure 4: Grand mean from 8 subjects for the regular anapest
condition with grand means for the two variants of the uncertain
condition superimposed. Case with 3rd beat present in red and
case with 3rd beat missing in blue.
In the third interval, however, there was a radical change in the
morphology of the ERP. In the 50% uncertain case with 3rd beat
present the regular N2 was suppressed and an early P3 appeared
(labelled P3a) at about 300 ms with amplitude about 1 V
followed by a later negativity (labeled N3) at about 400 ms with
an amplitude of about 2.5 V. For the P3a a three dipole solution
was attempted with a bilateral posterior source and a single
anterior source (Talairach-Tournoux coordinates, X=-38.6,+38.6,
Y=-57.9, Z=3.8, and X=-9.4, Y=36.3, Z= 17.7, RV = 3.8%).
However, this was not considered satisfactory as the location of
the bilateral sources in medial temporal lobe were not within
11mm of gray matter. The single anterior source located at the
juncture between medial frontal (BA9) and anterior cingulate
cortex (BA32) could alone account for the P3a with RV = 13.8%.
The N3 could be accounted for by a bilateral source in
temporoparietal cortex (Talairach-Tournoux coordinates, X=-
39.5,+48.3, Y=-37,-30.2, Z=31.8,23.5, RV = 5.5%). In this case
the symmetry condition was relaxed and the right source was
more lateral, anterior and deeper than the left. However both
sources were located in BA40 within the inferior parietal lobule.
For the 50% uncertain condition with 3
rd
beat missing there was
an eN1 at about 170 ms which had a more lateralised distribution
similar to that of the N150 but a reliable source analysis was not
obtainable. The P2/N2 was also supressed in this condition and
was followed by a later P3 (labelled P3b) which has a similar
latency as the P3 in the regular anapest, but with enhanced
amplitude. For the fourth interval the morphology of all three
conditions is again similar except that the amplitude of the eN1
was enhanced for the 50% uncertain 3rd beat present case. The
peak latency of this eN1 was about 150 ms.
For the active condition only four of the eight subjects were able
to carry out the task to a sufficient degree of skill, i.e. were able to
maintain good synchrony without significant flexor activity, thus
only these subjects were included in the analysis of the active
ICMPC8, Evanston, IL, USA August 3-7, 2004
214


condition. However, comparison of the grand mean of these four
with the overall grand mean shows them to be representative.

Figure 5: Grand mean (centred at FCz) for the active condition
for 4 skilled subjects compared with averaged EMG and force
responses.
The morphology of the first two intervals (Figure 5) are
comparable to that of the hybrid SRP/MRPs from Praamstra et al
(2003) as would be expected. For the third and fourth interval
however the morphology of the potentials more closely resembles
the pure MRP such that a PMN, RAN and PMP can be identified,
even though the averages were stimulus locked. This result is
consistent with the good performance of the four subjects in
maintaining accurate synchrony as can be seen in the well-
localised EMG and force responses. In the fourth interval the
PMN showed a double peak indicative of a more complex internal
structure. This may be related to the fact that the 4th interval is a
pure cycle of continuation, and hence they were labeled cPMNa,b
(respectively with latencies of about 270 ms and 310 ms) to
distinguish them from the synchronisation PMN. Similarly the
RAN in the gap just prior to the 1st click, which was more sharply
focussed in time, is likely more of a pure MRP hence it was
labeled cRAN.

Figure 6: Grand mean for the active condition for 4 skilled
subjects compared with their corresponding mean for the passive
condition.
Examination of the scalp potential distribution showed that the
latter part of the premovement negativity was focussed over left
central electrodes (approximately C1) consistent with it being a
correlate of activity in primary motor cortex. EMG started during
the PMN about 200 ms before target time, followed by the force
onset at about 150 ms before target and onset of RAN between
about 80 to 60 ms before target. EMG reached a peak at about 90
ms before target followed by the peak force almost exactly on
target. In the 4th beat the RAN peaked about 10 ms after the
target. The cRAN appeared to peak just before the target by about
25 ms but it may be the case that its continuation past the target
was masked by the early auditory waves. In order to directly
compare active and passive conditions waveforms are
superimposed in Figure 6. In the 3
rd
interval before the missing
beat there was a considerable temporal and spatial overlap
between the N2 and PMN. In the 4th interval the eN2 was
temporally aligned with the cPMNb, but the eN2 of Figure 2 (8
subjects) also shows a double peak.
4. DISCUSSION
That the N1 was reduced in magnitude from the random to the
regular condition and shows adaptation within the anapest is
consistent with previously established literature indicating that the
amplitude is inversely related to stimulus repetition rate, most
likely due to the refractoriness of the N1. For the random
condition the mean rate was between 1 and 0.5 Hz whereas for the
anapest it was between 2 and 1 Hz. Of more interest was the
observation that of the tangential and radial components of the
N1, the radial component (N150) was more prominent in the
anapest condition. This could be simply interpreted as the N150
being less susceptible to adaptation or it could be interpreted as it
representing a more active process associated with regularity. The
fact that the emitted N1s peaked in the uncertain conditions at
about 150 ms and that they had a more lateral distribution similar
to the N150, supports an interpretation whereby the generator of
the N150 is active and that it is the primary source for the eN1.
However a reliable source analysis was not obtainable from the
emitted potentials and so a possible association must remain
purely conjectural at this stage.
The spatio-temporal overlap of the N2 with the PMN when
comparing active and passive conditions is suggestive that the
auditory N2 in the conditions presented here may be movement
related, or at least include a component which is movement
related. Such an interpretation of the N2 being movement related
would be consistent with a location of the N2 generator(s) in the
frontal lobe. It would also be controversial though as previous
studies have located generators of the various negativities
following the N1/P2 complex, including the mis-match negativity

(MMN) and slow wave (SW), in the temporal lobe (Sherg et al.
1989). However, frontal lobe generators have also been postulated
for the late auditory potentials (Naatanen and Picton, 1987) and so
a frontal source for the N2 in this case is not implausible.
However, the source analysis for the regular N2s was ambiguous
between SMA and ACC. In retrospect the simple bilateral model
may have been inappropriate and a more complex model
including both bilateral temporal sources and a source near the
midline in SMA (as for the random N2) would give a more
plausible account of the N2. This would be consistent with
imaging studies which show activation of SMA in continuation,
and the anapest rhythm does involve one cycle of continuation.
Conversely an ACC source would seem less plausible as the task
did not involved error detection or monitoring (Praamstra et al.,
2003).
ICMPC8, Evanston, IL, USA August 3-7, 2004
215


If the above interpretation is correct, that activation of SMA is
centrally involved in beat induction, then it needs to be explained
what is different with the random case which also indicated SMA
activation. One possibility could be that both random and regular
rhythms evoke the same basic auditory-motor mechanism,
possibly related to a primitive orienting response (Naatanen and
Gaillard, 1983). The basic response however could be
suplemented with a rapid learning mechanism which forms a
representation of the stimulus interval. Thus the apparent
integration in the magnitude of the N2 over the anapest may be
the result of long term potentiation (LTP) in the learning
mechanism, possibly involving the hippocampus and basal
ganglia. Such a learning mechanism would be capable of
generating an expectation or intention on the basis of the interval.
An active component to the regular evoked N2 thus provides an
account of the emitted N2 in the gap. If the mechanism is
generating a "pulse" of activity then it should be visible even
without an explicit stimulus. The wave which we have identified
as eN2 has a latency of 300 ms which is within 20 or 30 ms of the
evoked N2. The amplitude of the eN2 is about 1.0 V which
added to the random N2 gives a magnitude comparable to the
regular N2. Thus the eN2 could plausibly represent a continuation
of the expectation. This view is strengthened by the temporal
alignment of the eN2 with cPMNb.
We have already discussed the possible association of the eN1
with the N150 whereby the N150 could be a correlate of an active
process in auditory cortex. Irrespective of whether this association
holds up or not there are two possible mechanisms which could
underly an active N1 component. The first is that the active
component is self-generated in auditory cortex. As is reviewed
elsewhere (Todd et al 2002) there is now a considerable body of
evidence that many neurones in auditory cortex have receptive
fields (RFs) which are tuned for modulation frequency between
about 0.5 and 20 Hz and that collectively they compute a
modulation power spectrum. The RFs come is a variety of species
with both low-pass and band-pass types being present. Of
particular relevance to our account is the fact that band-pass RFs
are associated with "ringing" or damped oscillations. Thus the
eN1 may be a correlate of ringing of band-pass RFs in auditory
cortex. Given the fairly broad tuning (or heavy damping) of the
RFs one would expect a spread of activation in the population and
hence a dispersion in the temporal response, which is what is
observed in the eN1. The location of the eN1/N150 generators in
the lateral belt area of auditory cortex would also be consistent
with the documented modulation sensitivity of this region
(Rauscheker and Tian, 2000). This account is not precluded
though by the second possible mechanism, which is that the active
component is a response to the pulse generator via reciprocal
connections between SMA and auditory cortex. Indeed it is likely
that the two would work together. The modulation power
spectrum in the lateral belt area provides candidate beat intervals,
which for most metrical rhythms there are a number possible
(unlike simple metronome tracking), and the pulse generator,
informed by the natural frequencies of the body, reinforces one
beat interval in particular.
Turning now to the interpretation of the case when there is
uncertainty in the presence of the third click of the anapest
rhythm. We have noted in the results the dramatic change in
morphology of the potentials in the third interval even though, it
should be stressed, that when the 3rd click is present it is
physically identical to the regular anapest. This change in
morphology was accompanied by two more subtle changes, i.e. an
enhancement of the P2 for the first two intervals and a general
increase in negativity after the second N2 and prior to the 3rd
click.
Considering the subtle changes first, although we have not
provided an account here for the origin of the P2 it is established
in the literature that it is modulated by attention (Picton et al.,
1974). Hence one simple account is that the enhanced P2 reflects a
higher level of attention in the subjects for the uncertain condition.
The negativity has similarities with a contingent negative
variation (CNV) and therefore could be interpreted as a correlate
of a kind of "readiness for action" process consistent with a higher
level of attention. The change is morphology is principally
characterised by a suppression or at least a masking of the N2 by
the appearance of an early P3, which could be accounted for by a
prefrontal source, followed by a later N3 localised in bilateral Tpt.
Thus far we have placed the N2 and SMA at the centre of our
account. Its disruption by the P3/N3 complex we take therefore to
indicate that a quite distinct mechanism is being activated under
this condition. The fact that the early P3 appears only after the
detection of the stimulus present may be taken to indicate that it is
a correlate of distributed process in prefrontal cortex involved in
the detection of uncertain stimuli in the context of heightened
attention and a prior expectation or readiness for action. As well
as detection, the distributed process associated with the P3 may
facilitate an action (in the general sense of the word) contingent
on the detection.
The PPC is thought to play a role, in conjunction with the
cerebellum and premotor cortex, in the transformation of sensory
to motor coordinates for sensory-guided action (Stein, 1995). At
least two areas within PPC have been identified as auditory. The
first, located in the interparietal sulcus (IPS), is associated with
auditory spatial processing. The second auditory area is located in
the temporoparietal region (Tpt), which overlaps with the inferior
parietal lobule (IPL), and is associated more with temporal
processing. The source analysis located the N3 in the
temporoparietal area and hence we surmise that it is a correlate of
audio-motor processing, including a circuit involving the
cerebellum. In addition to the change in morphology in the third
interval the uncertain condition gives rise to an enhanced eN1 in
the fourth interval, and this could be explained by invigoration of
the pulse generator through a boost by the IPL input. The
alternative simpler explanation that the eN1 is enhanced due to
greater level of attention is not consistent with the fact the evoked
N1s are not enhanced.
Both the SMA and IPL circuits we have proposed have influence
upon primary motor cortex as well as indirectly through premotor,
and prefrontal cortex and cerebellum. Motor cortex controls the
musculoskeletal system through motor neurons in the spinal
chord. In the potentials for the active case there was evidence that
the later part of the PMN was consistent with it being a correlate
of activity in primary motor cortex that occurred during the onset
of EMG. Any contraction of the target muscles has propriceptive
and somatosensory (tactile) consequences that are conveyed back
ICMPC8, Evanston, IL, USA August 3-7, 2004
216


to the brain to primary and secondary somatosensory cortex. The
RAN in the active case started just after the peak of EMG and
reached a peak just before or just after the target beat. This
suggests that the subjects here were using a somewhat different
synchronisation strategy to that described by Muller et al (2000)
who found a peak in the reafferance somewhat later after the
target.
5. CONCLUSION
In this paper we have presented data from an experiment to
investigate brain processes underlying beat induction. The data
support an interpretation whereby two distinct processes are active
during listening to metrical rhythms. The first process, associated
with the N2, seems to be completely automatic and may be
instantiated in a brain circuit including the SMA. The second
process, associated with the N3, is more attention dependent and
is only activated for rhythms in which the arrival of events is
uncertain and may be instantiated in a brain circuit involving the
IPL and Tpt.
In the introduction two alternative theories were outlined, the
attentional oscillator theory and the movement intention theory.
The interpretation we have outlined above is not consistent with
either of these in their simplest of forms. Advocates of the AO
theory, on the one hand, suppose that an attentional mechanism,
usually implemented as a network of oscillators, "resonates" to
regular rhythms and synchronizes its own period and phase with a
particular metrical level in the rhythm. Thus a beat corresponds to
a window of "attentional energy" that is maximal at the target.
This interpretation is difficult to reconcile with the notion of
attention as we have used it. According the AO theory the more
regular the rhythm, the sharper the "attentional resonance" yet our
data would suggest the opposite, i.e. the more regular the rhythm
the less the attentional processing. More attention is only brought
into play to deal with uncertain or unexpected events. The MI
theory, on the other hand, as implemented in Todd et al. (2002)
attempted to account for temporal tracking and beat induction
without reference to an internal pulse generation mechanism and
by means of externally guided action only, in conjunction with
positive feedback from reafferance. This position is difficult to
reconcile with the evidence that the N2/PMN includes generators
in SMA/ACC and not lateral premotor cortex as would be
expected if the beat were purely externally referenced. Given the
association of the SMA with internally cued actions (Passingham,
1993) then the more regular rhythms most likely make use of an
internal guidance mechanism.
The truth of the matter therefore lies somewhere in between the
two positions. The pulse generator we have proposed could be
interpreted as a kind of attentional mechanism and the emitted N1
could be viewed as a reflection of this mechanism if it were the
case that it was generated by via reciprocal connections between
lateral belt of auditory cortex and SMA. It is however primarily a
mechanism for internal generation of action through its influence
on the SMA. The current proposal is therefore a more general
version of the MI theory as it incorporates both major subcortical
motor control structures. When a rhythm is isochronous or highly
regular little attention is required to maintain an internal pulse or
active synchronization and automated circuits likely involving
basal ganglia and cerebellum can deal with the required
processing. For more complex rhythms involving syncopated or
unexpected events undoubtedly an attention dependent externally
guided mechanism comes into play. During active synchronization
both corollary discharge and reafference are available, which in
principle could provide the positive feedback to both subcortical
circuits required to sustain continuation without need for the
internal feedback.
Whilst the account we have developed is consistent with the data
presented it must be regarded as tentative at this stage until further
experiments are conducted. Investigations are needed of the effect
of variation in the parameters of beat rate, intensity, frequency and
rhythm complexity (not least syncopation) in order to substantiate
the proposals we have made. Additionally other imaging methods
are necessary to more accurately localise the hypothesised brain
areas involved.
6. REFERENCES
1. Large and Jones (1999). The dynamics of attending, Psych.
Rev. 106, 119-159.
2. Moelents, D. and Van Noorden, L. (1999). Resonance in the
perception of musical pulse, J. New Mus. Res. 28, 43-66.
3. Muller, K., Schmitz, F., Schnitzler, A., Freund, H.,
Aschersleben, G. and Prinz, W. (2000). Neuromangnetic
correlates of sensorimotor synchronisation, J. Cog. Neurosci.
12(4), 546-555.
4. Naatanen, R. and Picton, T. (1987). The N1 wave of the
human electric and magnetic response to sound: A review and
an analysis of component structure, Psychophysiol. 24, 375-
425.
5. Naatanen, R. and Gaillard, A.W. (1983). The orienting reflex
and the N2 deflection of the ERP, In A Gaillard & W Ritter
(eds), Tutorials in Event-Related Potential Research. North-
Holland: Amsterdam, pp 119-141.
6. Passingham, R. (1993). The frontal lobes and voluntary
action. Oxford University Press, Oxford.
7. Picton, T., Hillyard, S.A., Krausz, H.I. and Galambos, R.
(1974) Human auditory evoked potentials II: Effects of
attention, Electroencephal. Clin. Neurophysiol. 36, 191-199.
8. Praamstra, P., Turgeon, M., Hesse, C.W., Wing, A.M. and
Perrya, L. (2003). Neurophysiological correlates of error
correction in sensorimotor-synchronisation, Neuroimage 20,
1283-1297.
9. Rauschecker, J. and Tian, B. (2000). Mechanisms and
streams for processing of 'what' and 'where' in auditory
cortex, PNAS 97(22), 11800-11806.
10. Scherg, M., Vajsar, J. and Picton, T. (1989). A source
analysis of the late auditory evoked potentials,. J. Cog.
Neurosci. 1(4), 336-355.
ICMPC8, Evanston, IL, USA August 3-7, 2004
217


11. Stein, J. (1995) "The PPC, the cerebellum and the visual
guidance of movement". In F.W. Cody (Ed.) Neural Control
of Skilled Human Movement. Portland Press: London. pp 31-
49
12. Todd, N.P.M, O'Boyle, DJ and Lee, CS (2002) A
sensorimotor theory of beat induction and temporal tracking,
Psych. Res. 36: 11191134.
ICMPC8, Evanston, IL, USA August 3-7, 2004
218