ral
ssBioMed Cent
BMC Neuroscience
Open Acce
Research article
Auditory temporal processing in healthy aging: a
magnetoencephalographic study
Peter Sörös*
1
, Inga K Teismann
1,2
, Elisabeth Manemann
1
and
Bernd Lütkenhöner
3
Address:
1
Department of Neurology, Münster University Hospital, Albert-Schweitzer-Str. 33, 48149 Münster, Germany,
2
Institute for
Biomagnetism and Biosignalanalysis, University of Münster, Malmedyweg 15, 48149 Münster, Germany and
3
Department of Otolaryngology,
Head and Neck Surgery, Münster University Hospital, Kardinal-von-Galen-Ring 10, 48149 Münster, Germany
Email: Peter Sörös* - peter.soros@gmail.com; Inga K Teismann - i.teismann@gmx.de; Elisabeth Manemann - manemann-e@gmx.de;
Bernd Lütkenhöner - bernd.lutkenhoner@uni-muenster.de
* Corresponding author
Abstract
Background: Impaired speech perception is one of the major sequelae of aging. In addition to
peripheral hearing loss, central deficits of auditory processing are supposed to contribute to the
deterioration of speech perception in older individuals. To test the hypothesis that auditory
temporal processing is compromised in aging, auditory evoked magnetic fields were recorded
during stimulation with sequences of 4 rapidly recurring speech sounds in 28 healthy individuals
aged 20 – 78 years.
Results: The decrement of the N1m amplitude during rapid auditory stimulation was not
significantly different between older and younger adults. The amplitudes of the middle-latency P1m
wave and of the long-latency N1m, however, were significantly larger in older than in younger
participants.
Conclusion: The results of the present study do not provide evidence for the hypothesis that
auditory temporal processing, as measured by the decrement (short-term habituation) of the major
auditory evoked component, the N1m wave, is impaired in aging. The differences between these
magnetoencephalographic findings and previously published behavioral data might be explained by
differences in the experimental setting between the present study and previous behavioral studies,
in terms of speech rate, attention, and masking noise. Significantly larger amplitudes of the P1m and
N1m waves suggest that the cortical processing of individual sounds differs between younger and
older individuals. This result adds to the growing evidence that brain functions, such as sensory
processing, motor control and cognitive processing, can change during healthy aging, presumably
due to experience-dependent neuroplastic mechanisms.
Background
Auditory temporal processing, the precise detection of the
auditory temporal processing has been suggested as a
symptom in disorders as diverse as dyslexia [2] and
Published: 7 April 2009
BMC Neuroscience 2009, 10:34 doi:10.1186/1471-2202-10-34
Received: 8 October 2008
Accepted: 7 April 2009
This article is available from: http://www.biomedcentral.com/1471-2202/10/34
© 2009 Sörös et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Page 1 of 9
(page number not for citation purposes)
temporal features of sounds, is a prerequisite for speech
perception and reading (for a review, [1]). A deficit of
autism [3]. Moreover, impaired speech perception is one
of the major sequelae of aging [4]. Several lines of evi-

BMC Neuroscience 2009, 10:34 http://www.biomedcentral.com/1471-2202/10/34
dence suggest that not only peripheral high-frequency
hearing loss, but also central deficits of auditory temporal
processing contribute to the deterioration of speech per-
ception in older individuals [5,6].
Numerous behavioral studies indicated an impairment of
auditory temporal processing in healthy aging. Older lis-
teners have more difficulties than younger listeners in
detecting short gaps within speech and non-speech stim-
uli, a widely used behavioral technique for the assessment
of auditory temporal resolution [7]. Age-related differ-
ences in gap detection appear to be independent of
peripheral hearing loss because performance in gap detec-
tion is not correlated with audiometric thresholds [8,9].
Of particular importance for the perception of speech is
that the discrimination of voice onset times can be
impaired in the elderly [10]. The voice onset time refers to
the time interval between the release of a consonant and
the onset of vocal fold vibrations. Older listeners also
show poorer performance in more complex behavioral
tasks which evaluate the ability to discriminate changes in
the timing of successive auditory stimuli [11,12]. Similar
to gap detection, hearing loss does not significantly influ-
ence the performance in these tests [11,12]. There is evi-
dence that these age-related deficits start relatively early in
life. Deficits of temporal processing were already found in
a group of 40–55 year-old individuals [13].
Considering these behavioral findings, we hypothesized
that the cortical processing of rapidly recurring sounds,
similar to the succession of syllables in speech, is impaired
in the elderly. To test this hypothesis, we recorded audi-
tory evoked magnetic fields (AEF) in healthy volunteers
aged 20 to 78 years during short series of speech sounds
using magnetoencephalography (MEG). MEG is an excel-
lent tool for studying rapid temporal processing due to its
high temporal resolution in the range of milliseconds. The
recording of AEFs has a high reliability (test-retest repro-
ducibility [14,15]) and a high validity (consistency with
intracranial recordings [16,17]).
Data analysis focused on two major AEF components, the
middle-latency P1m and the long-latency N1m, both orig-
inating from the superior temporal plane [16,18,19]. The
N1m component is the strongest and most reliable com-
ponent of the auditory evoked responses and is mainly
influenced by temporal and physical aspects of a given
stimulus [20]. We determined not only the latency and
amplitude of the N1m and the location of the underlying
cortical source, but examined also the decrement of the
response amplitude that occurred when presenting series
of four stimuli at short intervals, separated by a prolonged
silent period [20]. The decrement of auditory evoked
believed to represent cortical filtering of irrelevant input
[25]. Deficient encoding (or gating) of repeated stimuli
might result in increased responses to repeated stimuli, as
shown in patients with schizophrenia [26,27].
Results
N1m decrement
Averaged MEG waveforms for a subgroup of younger
adults (n = 14; mean age: 23 years; age range: 20 – 27
years) and a subgroup of older adults (n = 9; mean age: 66
years; age range: 60 – 78 years) are shown in Fig. 1. These
waveforms represent the amplitude of the dipole moment
for the source location of the first N1m peak over the
entire epoch (-50 ms – 2000 ms). A prominent response,
peaking about 100 ms after stimulus onset (N1m), and a
preceding wave, peaking about 50 ms after stimulus onset
(P1m), are visible in the averaged waveforms of both
groups. The relative amplitude of the second N1m (the
Averaged AEF waveformsFigure 1
Averaged AEF waveforms. Averaged auditory evoked
magnetic fields in 14 younger (A, age range: 20 – 27 years)
and 9 older adults (B, age range: 60 – 78 years). The first P1m
and N1m responses are marked. The black waveforms rep-
resent the median and the grey area the upper and lower Page 2 of 9
(page number not for citation purposes)
responses with rapid stimulation, also known as habitua-
tion [21,22], sensory gating [23,24], or attenuation, is
95% nonparametric bootstrapped confidence intervals.

BMC Neuroscience 2009, 10:34 http://www.biomedcentral.com/1471-2202/10/34
ratio between the amplitudes of the second and the first
N1m response) was not significantly different between
younger adults (median = 40%, range 0 – 77%) and older
adults (median = 37%, range 20 – 51%; p = 0.69, Mann-
Whitney test).
Fig. 2 depicts the relative amplitude of the second N1m
response as a function of age in the entire sample (n = 28;
mean age: 40 years; age range = 20 – 78 years). No signif-
icant correlation between the relative amplitude of the
N1m and age was found.
P1m amplitude
Amplitudes of the first P1m are significantly larger in
older (median = 13 nAm, range = 10 – 26 nAm) than in
younger participants (median = 2 nAm, range = 0 – 10
nAm; p < 0.001, Mann-Whitney test). In the entire sam-
ple, the amplitudes of the first P1m were significantly cor-
related with age (ρ = -0.72, p < 0.001, Spearman's rank
correlation; Fig. 3).
N1m amplitude
Amplitudes of the first N1m are significantly larger in
older (median = 37 nAm, range = 21 – 55 nAm) than in
younger individuals (median = 22 nAm, range = 12 – 62
nAm; p = 0.03). In the entire sample, the amplitudes of
the first N1m were significantly correlated with age (ρ =
0.42; p = 0.027; Spearman's rank correlation; Fig. 4).
P1m and N1m latencies
The latencies of the first P1m and the first N1m were not
significantly different between older and younger adults.
The median P1m latency for older vs. younger individuals
was 44 ms (range 37 – 57 ms) vs. 39 ms (range 30 – 57
ms; p = 0.22, Mann-Whitney test). The latency of the first
N1m response was 94 ms (81 – 124 ms) in older and 101
ms (91 – 114 ms) in younger adults (p = 0.23, Mann-
Whitney test). No significant correlations were found
between age and the latencies of the first P1m and the first
N1m when analyzing the entire sample (data not shown).
Relative amplitude of the second N1m as a function of ageFigure 2
Relative amplitude of the second N1m as a function
of age. No significant association between the N1m decre-
ment (the relative amplitude of the second N1m to the first
0
25
50
75
0 25 50 75 100
age (years)
r
e
l
a
t
i
v
e

a
m
p
l
i
t
u
d
e

o
f
s
e
c
o
n
d

N
1
m

(
%
)
P1m amplitude as a function of ageFigure 3
P1m amplitude as a function of age. P1m amplitudes are
significantly larger in older than younger participants (linear
regression, R
2
= 0.56, F(1,26) = 32.78, p < 0.001). The black
line represents the linear regression line and the dashed lines
the confidence intervals.
0
-10
-20
-30
0 25 50 75 100
age (years)
P
1
m

a
m
p
l
i
t
u
d
e

(
n
A
m
)
N1m amplitude as a function of ageFigure 4
N1m amplitude as a function of age. N1m amplitudes
tend to be larger in older individuals (linear regression, R
2
=
0.13, F(1,26) = 3.77, p = 0.06). The black line represents the
linear regression line and the dashed lines the confidence
0
25
50
75
0 25 50 75 100
age (years)
N
1
m

a
m
p
l
i
t
u
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(
n
A
m
)Page 3 of 9
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N1m) and age was found. intervals.

BMC Neuroscience 2009, 10:34 http://www.biomedcentral.com/1471-2202/10/34
Source locations
No significant correlation between age and source loca-
tion and was found. Moreover, the source location was
not significantly different between age groups.
Hearing thresholds
Hearing thresholds for the speech stimulus used in the
experiment were determined immediately before the
MEG recordings on a relative dB scale. Hearing thresholds
were 2.8 ± 5.8 (mean ± standard deviation) dB for the
younger group and 8.1 ± 4.9 dB for the older group. Hear-
ing thresholds tend to be higher in older individuals (Fig.
5A), but the effect is small (subjective hearing loss was an
exclusion criterion). Participants with larger relative
amplitude of the second N1m (i.e., with smaller decre-
ment of the second N1m) tend to have lower hearing
thresholds (Fig. 5D). No significant correlation was found
between P1m and N1m amplitudes and hearing thresh-
olds (Fig. 5B, 5C).
Discussion
The results of the present study do not support the
hypothesis that cortical processing of rapidly recurring
speech sounds is impaired in healthy adults without sub-
jective hearing impairment. The cortical processing of
individual sounds, in contrast, differed between younger
and older individuals and was characterized by signifi-
cantly larger amplitudes of the middle latency P1m and
the long latency N1m wave in older compared to younger
participants.
N1m decrement
The N1/N1m response is characterized by a pronounced
amplitude decrease during repetitive stimulation [20].
When identical auditory stimuli are presented in pairs or
short sequences (i.e., in a short-term habituation experi-
ment), the second N1/N1m peak is considerably smaller
than the first peak. Grand averages of electric [28,21,22]
and magnetic recordings [29-31,15,32-34] demonstrate a
decrease of the second N1/N1m amplitude to less than
50% of the amplitude of the first response. This amplitude
decrease is frequently termed habituation [21,22] or sen-
sory gating [23]. For the present report, however, we pre-
fer the descriptive term "decrement" [15,32].
In the present study, the decrement of the N1m wave dur-
ing a sequence of four vowel stimuli (ISI = 450 ms,
sequence presentation rate = 0.2 Hz), was not significantly
different between younger and older participants in a pas-
sive listening condition and in an environment with low
acoustic noise. By contrast, two earlier ERP studies using
pure tones of 50 ms duration [35] or harmonically
enriched tones (75 ms duration) [36] provided evidence
smaller in older than younger adults. But there are impor-
tant methodological differences. In the study performed
by Papanicolaou et al. the participants attended to the
stimuli [35], whereas in the present study they watched a
self-selected silent movie that drew their attention and
kept it on a relatively stable level. Selective attention has
been shown to increase the amplitudes and the latencies
of long-latency auditory evoked potentials [37-39]. In the
study of Fabiani et al. [36], ERPs were recorded while the
participants were reading a book, ignoring the stimuli.
Although the study was similar to ours in this respect, the
results are not easily comparable, because Fabiani et al.
used the 200 ms time interval before the first stimulus in
a sequence also as the baseline for the other stimuli in the
sequence and did not correct for a baseline shift during
the stimulus sequence [36].
As noted in the introduction, behavioral data indicate that
the processing of rapid acoustic stimuli is impaired in the
elderly [11,12,9,7,8]. The differences between our find-
ings and previously published behavioral data might be
explained, at least in part, by differences in the experimen-
tal settings. The experimental parameters used here dif-
fered from a natural listening situation. Although the
magnetically shielded room containing the MEG system is
not sound-proof, it attenuates external acoustic noise.
Moreover, no competing sounds were presented during
the acoustic stimulation. A major complaint of older indi-
viduals, however, is impaired speech perception in the
presence of additional, distracting speakers. Numerous
studies provided evidence that older listeners, even with
relatively intact peripheral hearing, have more difficulties
in understanding speech than younger adults when
speech stimuli are masked by speech or noise [40,41].
The present study used a fixed onset-to-onset interstimu-
lus interval (ISI) of 450 ms (presentation of 2.2 stimuli/s).
This presentation rate was considerably lower than the
rate at which individual sounds in normal speech are pro-
duced (5 – 10 syllables/s) [42]. In a pilot study, we used
short (20 ms) sine tones and stimulated with an onset-to-
onset ISI of 220 ms [43]. The short ISI resulted in an ill-
defined baseline between evoked responses due to the
superimposition of response waveforms, which made the
quantification of P1m and N1m amplitudes unreliable.
We cannot rule out the possibility that a faster presenta-
tion rate than used in the present study (i.e., > 2.2 Hz)
might reveal significant differences between the N1m dec-
rement in younger and older individuals. Repetition fre-
quency is crucial because older listeners have more
difficulties in accurately detecting words when the speech
rate is faster than normal (for a review, see [44]).Page 4 of 9
(page number not for citation purposes)
that the decrement of the P1-N1 and N1-P2 amplitudes
[35] and the baseline-to-peak N1 amplitude [36] is

BMC Neuroscience 2009, 10:34 http://www.biomedcentral.com/1471-2202/10/34
P1m and N1m amplitudes
The finding that P1m amplitudes are significantly larger in
detected in older adults [45-47,36]. Similarly, a more
recent study used MEG to investigate auditory processing
Hearing thresholdsFigure 5
Hearing thresholds. A) Hearing thresholds for the vowel /a/ as a function of age in a relative dB scale. The line represents
the linear regression line (R
2
= 0.16, F(1,16) = 3.04, p = 0.1). B) Hearing thresholds for the vowel /a/ as a function of the first
P1m amplitude. Linear regression: R
2
= 0.05, F(1,16) = 0.94, p = 0.35. C) Hearing thresholds for the vowel /a/ as a function of
the first N1m amplitude. Linear regression: R
2
= 0.08, F(1,16) = 1.44, p = 0.25. D) Hearing thresholds for the vowel /a/ as a
function of the relative amplitude of the second N1m. Linear regression: R
2
= 0.18, F(1,16) = 3.42, p = 0.08.
age (years)
t
h
r
e
s
h
o
l
d

(
d
B
)
20 30 40 50 60 70 80
−
1
0
0
5
1
5
P1m amplitude (nAm)
t
h
r
e
s
h
o
l
d

(
d
B
)
−25 −20 −15 −10 −5
−
1
0
0
5
1
5
N1m amplitude (nAm)
t
h
r
e
s
h
o
l
d

(
d
B
)
20 30 40 50
−
1
0
0
5
1
5
rel. N1m amplitude (nAm)
t
h
r
e
s
h
o
l
d

(
d
B
)
0 20406080
−
1
0
0
5
1
5Page 5 of 9
(page number not for citation purposes)
older than younger individuals corroborates earlier
reports. Using AEPs, enhanced P1 components were
of elderly individuals and found larger P1m amplitudes
[48].

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Different mechanisms may contribute to increased P1/
P1m amplitudes in older individuals. In aged mice with
high-frequency hearing loss, the cortical representation of
higher frequencies decreased while lower and middle fre-
quencies became over-represented [49]. Thus, the loss of
cochlear hair cells observed in human aging is probably
accompanied by the reorganization of the auditory cortex
resulting in a larger cortical representation of the fre-
quency bands of speech [50], and therefore larger AEF
amplitudes. A larger representation of speech sounds in
aging is supposed to be associated with larger amplitudes
of AEFs, representing the number of synchronously active
neurons. In our study, however, a subjective hearing defi-
cit was an exclusion criterion, and older participants had,
on average, only slightly higher audiometric thresholds
than younger participants. An alternative explanation for
the larger P1m and N1m amplitudes in elderly humans is
an impaired GABAergic neurotransmission [51,47],
which would result in decreased subcortical and intracor-
tical inhibition as demonstrated in aged rats [52].
We found significantly larger N1m amplitudes in older
than in younger individuals (p = 0.03; Mann-Whitney U
test). Moreover, the amplitudes of the first N1m were sig-
nificantly correlated with age (ρ = 0.42; p = 0.027; Spear-
man's rank correlation). As the statistical analysis
comprised multiple comparisons, these results have to be
interpreted with caution, though. Previous studies report-
ing data on age-related changes of the N1/N1m amplitude
were contradictory. Some investigators found no signifi-
cant N1/N1m amplitude differences between younger
and older adults [45,48], others found an enhanced N1m
component [53]. Differences in the experimental setting
(speech vs. pure tone stimuli of different frequencies,
attentive vs. passive listening) complicate the comparison
of these results.
Methodological considerations
The estimation of P1m and N1m amplitudes might have
been complicated by at least two factors, brain atrophy
and increased hearing thresholds in aging. Brain atrophy
is frequently found in older individuals [54,55] and may
result in a deeper location of the P1m and N1m sources.
Brain atrophy, therefore, might interfere with the quanti-
fication of source strengths because deeper sources tend to
be estimated stronger than more superficial sources
[56,57]. However, it is unlikely that brain atrophy intro-
duced a considerable bias because no significant associa-
tion between age and source location was found.
Another point to be considered is that all stimuli were pre-
sented at an intensity of 60 dB above the individual hear-
ing threshold to achieve a comparable level of activation
hearing thresholds received physically stronger stimuli
than those with lower thresholds. While older individuals
tended to have higher hearing thresholds than younger
adults (p = 0.1; Mann-Whitney U test), we did not find a
significant association between P1m/N1m amplitudes
and hearing thresholds (Fig. 5), corroborating earlier ERP
results [58]. For the present study we recruited healthy
individuals without subjective hearing impairment, and
we assured that their hearing threshold for the vowel stim-
ulus was in the normal range, but we did not perform
pure-tone audiometry. As a consequence, we cannot
exclude that some of our participants might have had a
moderate hearing loss at the frequencies corresponding to
the higher formants in the speech signal. However, the
effect of a possible high-frequency hearing loss on the
results of our MEG recordings can be expected to be small,
because the sound transmission between the speaker out-
side the magnetically shielded room and the ear piece
inside the room attenuated higher frequencies anyway
(see Methods).
Finally, recruiting healthy seniors with normal or near-to-
normal hearing who qualified for an MEG experiment (no
implanted metal or stimulation devices that may cause
electromagnetic artefacts) was challenging for us. Thus,
the sample size is relatively small (n = 14 in the group of
younger, n = 9 in the group of older adults), and the con-
clusions based on the current study are limited by the
small sample size and by the unequal age distribution of
this sample. For future studies of auditory processing in
healthy aging, a larger sample of participants is desirable,
equally distributed over the adult life span. Such studies
are expected to determine the age of onset and the further
development of age-related changes in auditory process-
ing.
Conclusion
These results suggest that healthy aging is not necessarily
associated with changes in the decrement of the major
auditory evoked component, the N1m wave. The cortical
processing of individual sounds, in contrast, was different
between younger and older individuals, characterized by
significantly larger amplitudes of the middle-latency P1m
wave in older participants. All MEG recordings reported
here were performed in a low-noise environment while
participants watched a silent movie, although age-related
central auditory disorders are often more pronounced in
noisy situations. Thus, future studies on auditory tempo-
ral processing in aging should include auditory stimuli
masked by noise [59,60].
Methods
ParticipantsPage 6 of 9
(page number not for citation purposes)
in the brain, basically independent of individual hearing
thresholds. As a consequence, individuals with higher
Twenty-eight healthy, right-handed adults without subjec-
tive hearing impairment were included (15 men, 13

BMC Neuroscience 2009, 10:34 http://www.biomedcentral.com/1471-2202/10/34
women, mean age = 40 years, age range = 20 – 78 years).
All participants had normal audiometric thresholds for
the auditory stimulus tested here. Participants gave their
written informed consent to participate in the study. The
study protocol was reviewed and approved by the
Research Ethics Board, Medical Faculty, University of
Münster, Germany. MEG recordings of some of the partic-
ipants were published earlier as part of a healthy control
group in a paper on auditory processing in stroke [32] and
in a paper on the neurochemical basis of human cortical
auditory processing [15].
Auditory stimulation
The German vowel /a/ with a duration of 260 ms and a
fundamental frequency of 234 Hz served as stimulus
(unsmoothed, frequency of the first formant (F1) = 835
Hz, F2 = 1205 Hz). The stimulus was spoken by a female
speech-language pathologist, recorded in a sound-proof
chamber and stored on a computer. During the MEG
recording, 160 sequences (or trains) comprising 4 repeti-
tions of this stimulus were presented. The onset-to-onset
interstimulus interval between the stimuli in a sequence
was 450 ms. The onset-to-onset interval between
sequences was pseudo-randomized between 4 s and 5 s.
As the electromagnetic activation of the auditory cortex
lasts for approximately 400 ms after the onset of a single
transient stimulus, an interstimulus interval of 450 ms (or
2.2 stimuli/second) was chosen to avoid overlap between
successive brain responses. The onset-to-onset interval
between sequences (4.5 s) is long enough to allow a sub-
stantial recovery of the N1m component before the onset
of the following sequence [22]. Immediately before each
MEG measurement, the individual hearing thresholds
were determined for the stimuli. A non-significant trend
was observed for increased hearing thresholds in higher
age (ρ = 0.43, p = 0.075, Spearman's rank correlation).
The stimuli were delivered to a silicon earpiece in the right
ear via speakers outside the shielded room and a plastic
tube of 6.3 m length. Measurements with a 2 cm
3
ear-sim-
ulator (Model 4157, Brüel and Kjær, Nærum, Denmark)
at the end of the plastic tubing indicated that the transmis-
sion of acoustic stimuli is relatively unimpaired up to a
frequency of about 1500 Hz [61,62]. Spectra of narrow-
band (1131 – 2262 Hz) and broad-band stimuli (400 –
6400 Hz) before and after passing through the sound
delivery system (Fig. 3 in reference [62]) and the impulse
response of the sound delivery system (Fig. 1 in reference
[63]) were shown in earlier articles of our group. All stim-
uli were presented at an intensity of 60 dB above the indi-
vidual hearing threshold.
MEG data acquisition
Recordings were performed using a 37-channel biomag-
published previously [15]. The participants were in a right
lateral position with the body supported by a vacuum
cushion to minimize head and body movements during
the measurement. The sensor array was positioned over
the left superior temporal cortex as closely as possible to
the subject's head. Participants were instructed not to
move their head, to stay awake, and to keep their eyes
open. Participants listened passively to the stimuli to min-
imize the influence of inter-individual differences in
attention and concentration. To ensure a stable passive lis-
tening condition, subjects watched a self-selected silent
video which attracted their attention.
MEG data analysis
After excluding epochs contaminated by artifacts, the
magnetic waveforms were averaged and band-pass filtered
(0.01–40 Hz). A single equivalent current dipole was cal-
culated for each sampling point. To assess the cortical
source of the N1m, dipole moments were averaged for a
30 ms time window around the N1m peak following the
first stimulus in a sequence. This dipole was used to calcu-
late the amplitude of the dipole moment over the entire
epoch. For this calculation, the location and the direction
of the N1m dipole were assumed to be constant (fixed-
dipole approach). The N1m was identified as the strong-
est deflections in its typical latency range (70 – 150 ms).
Based on the dipole moment over time, the peak ampli-
tudes and peak latencies of the N1m responses were deter-
mined. In most participants, a baseline shift was detected
from the beginning of the first response to the fourth
response. A traditional baseline correction that uses a sin-
gle time window of e.g. 200 ms before stimulus onset [61]
would have resulted in confounded amplitude values. To
ensure accurate quantification of amplitudes, dipole
moments were therefore measured relative to a baseline
that was defined as the mean value before the onset of
each stimulus (-50 to 0 ms pre-stimulus) [15]. Baseline
activity was not significantly different between age groups.
In a subsequent step, the amplitude ratio of the second
and first N1m (termed the relative amplitude of the sec-
ond N1m) was calculated. To assess the variability of
dipole moments, bootstrapped 95% confidence intervals
were calculated over the entire epoch (Fig. 1).
Statistics
Statistical testing was carried out for (1) the entire group
of 28 participants and (2) two subgroups of younger (n =
14; mean age: 23 years; age range: 20 – 27 years) and older
participants (n = 9; mean age: 66 years; age range: 60 – 78
years). Data are presented as median and range. Differ-
ences between group means were assessed using the two-
tailed Mann-Whitney U test. To test for associations
between variables, Spearman's rank correlation was calcu-Page 7 of 9
(page number not for citation purposes)
netometer (Magnes I, BTi, San Diego, USA) in a magneti-
cally shielded room and sampled at a rate of 512.4 Hz as
lated. Statistical analyses were performed with the statisti-
cal language R for Mac OS X http://www.r-project.org.

BMC Neuroscience 2009, 10:34 http://www.biomedcentral.com/1471-2202/10/34
Authors' contributions
PS, IKT, EM, and BL designed the study, interpreted the
results, and drafted the manuscript. PS, IKT, and EM
recorded and analyzed the MEG data. All authors read and
approved the final manuscript.
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