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Original Title: Detrended Fluctuation Analysis of Resting EEG in Depressed

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www.elsevier.com/locate/clinph

outpatients and healthy controls

Jun-Seok Lee a, Byung-Hwan Yang b, Jang-Han Lee c,*, Jun-Ho Choi b,

Ihn-Geun Choi d, Sae-Byul Kim e

a

Department of Psychiatry, Kwandong University College of Medicine, Myongji Hospital, 697-24 Hwajeong, Dukyang, Gyang,

Gyunggi 412-270, Republic of Korea

Department of Neuropsychiatry, Hanyang University College of Medicine, 17 Haengdang, Seongdong, Seoul 133-791, Republic of Korea

c

Department of Psychology, Chung-Ang University, 221, Heukseok-dong, Dongjak-gu, Seoul 156-756, Republic of Korea

d

Department of Neuropsychiatry, Hallym University Han-Gang Sacred Heart Hospital, Seoul 150-719, Republic of Korea

e

Korean Intellectual Property Oce, 920 Dunsandong, Seogu, Daejeon 302-701, Republic of Korea

Accepted 4 August 2007

Available online 24 September 2007

Abstract

Objective: Recent ndings have demonstrated that the EEG possesses long-range temporal (auto-) correlations (LRTC) in the dynamics

of broad band oscillations. The analysis of LRTC provides a quantitative index of statistical dependencies in oscillations on dierent time

scales. We analyzed LRTC in resting EEG signals in depressed outpatients and healthy controls.

Methods: The participants in this study were 11 non-depressed, age-matched controls, and 11 unmedicated unipolar depressed patients.

EEG data were obtained from each participant during 5-min resting baseline periods with eyes closed and then analyzed with detrended

uctuation analysis (DFA), a scaling analysis method that quanties a simple parameter to represent the correlation properties of a time

series. The scaling exponent, the result of DFA, provides a quantitative measure of LRTC from the EEG.

Results: The present study demonstrates that all the scaling exponents in depressed patients and healthy controls were greater than 0.5

and less than 1.0, regardless of condition. Furthermore, the scaling exponents of depressed patients have relatively higher values in whole

brain regions compared to healthy controls, with signicant dierences at F3, C3, T3, T4 and O1 channels (p < 0.05). Finally, a significant linear correlation was observed between the severity of depression and the scaling exponent over most of the channels, except O2.

Conclusions: These results suggest that the brain aected by a major depressive disorder shows slower decay of the LRTC, and that the

persistence of the LRTC of EEG in depressed patients was associated with the severity of depression over most of the cortical areas.

Signicance: The DFA method may broaden our understanding of the psychophysiological basis of depression.

2007 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Keywords: Major depressive disorder; EEG; Detrended uctuation analysis

1. Introduction

There is some evidence that the resting EEG may be a

useful tool in the study of depression. Patients diagnosed

with clinical depression have frequently exhibited increased

alpha and/or theta power (Nystrom et al., 1986; Pollock

Corresponding author. Tel.: +82 2 820 5851; fax: +82 2 816 5124.

E-mail address: clipsy@cau.ac.kr (J.-H. Lee).

and Schneider, 1990) as well as interhemispheric asymmetry (Schaer et al., 1983; Henriques and Dividson, 1990)

and hypocoherence in anterior regions (John et al., 1988;

Ford et al., 1986). These ndings for resting EEG in

depressed patients are based on morphologic analysis

which decomposes the component frequencies and amplitudes in the EEG oscillation.

In contrast to these conventional approaches in terms of

linear dynamics, alternative approaches were applied to the

EEG oscillations in the framework of non-linear dynamics.

1388-2457/$32.00 2007 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

doi:10.1016/j.clinph.2007.08.001

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It was assumed that the EEG within a particular psychophysiological state could be described by non-linear

dynamics and, therefore, could be characterized by non-linear analysis. With regard to this perspective, there has been

a sustained interest in analyzing the EEG within the context of non-linear dynamics (Rapp et al., 1989; Rapp,

1993; Palus, 1996). Recent ndings have shown that the

EEG possesses long-range temporal (auto-) correlations

(LRTC) in the dynamics of broad band oscillations (Parish

et al., 2004; Watters and Martin, 2004) and narrow bandpass ltered oscillations (Linkenkaer-Hansen et al., 2001;

Nikulin and Brismar, 2005). The analysis of LRTC provides a quantitative index of statistical dependencies in

oscillations on dierent time scales (as opposed to crosscorrelation analysis, which provides an index of statistical

dependencies between dierent channels) (LinkenkaerHansen et al., 2005). An essential feature of LRTC is their

power-law behavior, which indicates that the mechanisms

contributing to their build-up are similar at dierent time

scales (Nikulin and Brismar, 2005). The importance of

LRTC stems from the fact that their presence is thought

to be advantageous for a reliable transfer of information

in neuronal populations (Chialvo and Bak, 1999; Beggs

and Plenz, 2003).

The characteristics of non-linear dynamics in EEG oscillations in patients with depressive disorder have been noted

in several clinical studies (Nandrino et al., 1994; Thomasson et al., 2000). These studies suggest that mood be considered to be a psychophysiological state emerging from a

specic neuronal process revealed by non-linear analysis

methods. However, there has been a diculty in establishing the nature of the underlying non-linear process more

precisely as it could be due to a number of interrelated

methodological drawbacks. One of these drawbacks is the

dierentiation between non-linear dynamics and noisy

background in a spatially extended system (Grassberger,

1989; Mayer-Kress and Kaneko, 1989; Palus, 1996). In this

context the detrended uctuation analysis (DFA), invented

by Peng et al. (1992), has been established as an important

non-linear analysis technique for the detection of LRTC in

a non-stationary time series. DFAs advantages are its

enabling the detection of LRTC embedded in a non-stationary time series, as well as its avoidance of the spurious

detection of apparent LRTC that are the noise of a nonstationary time series (Kantelhardt et al., 2001; Watters

and Martin, 2004). Several studies have applied DFA to

EEG analysis and have convincingly demonstrated that

EEG has LRTC (Pereda et al., 1998; Popivanov and Mineva, 1999; Linkenkaer-Hansen et al., 2001). Recently, we

have shown that LRTC in EEG by DFA during a hypnotic

state diers signicantly from that with no hypnotic state

(Lee et al., 2007).

Assuming that the depression is related to a particular

psychophysiological state, we analyzed LRTC in resting

EEG signals in depressed outpatients and healthy controls,

using the DFA method. Another important aspect related

to the description of psychophysiological state of depres-

and severity of depression.

2. Methods and materials

2.1. Participants

Data were collected between June 2005 and November

2005 in Myongji Hospital Depression Clinic in Korea. Eleven right-handed unmedicated and unipolar depressed outpatients, 44 11 years of age (nine of which were females),

participated in the study. Illness severity was assessed prior

to EEG data collection. Depression symptoms were assessed

by the Beck depression inventory (BDI; Beck et al., 1961)

and the 17-item Hamilton depression rating scale (HDRS;

Hemilton, 1960). To be classied as depressed, two criteria

were to be met: (1) a BDI score of P10 and a HDRS score

of P14 at intake; and (2) a DSM-IV (American Psychiatric

Association, 1994) interview resulting in a diagnosis of a

major depressive episode.

Eleven right-handed healthy control participants

matched for age and sex were recruited through Internet

advertisement and screened for psychiatric or neurological

disease. To be classied as a non-depressed control, participants needed to score 69 on the BDI. In fact, the range of the

depressed group was 1443, with a mean of 28.36 on the BDI,

while the range of scores among the controls was 38, with a

mean of 4.36. Exclusion criteria for both groups consisted of:

(1) diagnosis of schizophrenia (or other psychotic disorders),

psychopathic personality disorder or alcohol/drug abuse or

dependence; (2) evidence of dementia, delusions, hallucinations or indication of a serious suicidal risk; (3) history of seizures, brain surgery, organic brain disease or organic

aective disturbance; (4) clinically signicant neurologic,

gastrointestinal, hepatic, renal, hematologic or respiratory

disease; (5) electroconvulsive therapy (ECT) history; (6)

use within the past 4 weeks of antidepressants (8 weeks in

the case of uoxetine), benzodiazepines, barbiturates, beta

blockers, cimetidine, clonidine, anticoagulants or any centrally active agent. The study was approved by the Institutional Review Boards of Kwandong University Myongji

Hospital. All participants gave their written informed consent before enrolling in the study.

2.2. EEG recordings and experimental conditions

The participants were seated in a comfortable armchair

in a sound-attenuated, dimly lit EEG room. After having

become accustomed to the atmosphere, the participants

were checked for a 5-min resting EEG collection with eyes

closed. To avoid any disturbances and interferences, the

recording room was shielded with copper. EEG were

recorded using silversilver chloride cup electrodes (Ag

AgCl) attached by collodion, on F3 and F4 (frontal), on

C3 and C4 (central), on T3 and T4 (temporal) and on O1

and O2 (occipital) scalp regions of the 1020 international

system (American Electroencephalographic Society, 1994).

All electrode impedances were below 5 kX. The EEG-measurement-device (LEX3208, LAXTHA Inc., Korea) settings were as follows: 256-Hz sampling rate, 12-bit

analog-to-digital (A/D) converter, 0.6-Hz high-pass lter,

46-Hz low-pass lter, and 60-Hz notch lter. The EEG

data were visually inspected for artifacts. Data contaminated with artifact were discarded.

2.3. Data analysis and statistics

The EEG data were successively segmented into consecutive 30 s epochs for DFA. The sequences of 10 30-s epochs of

each EEG served as the database. For each 30 s epoch, we

applied DFA according to the following algorithm (Peng

et al., 1995; Goldberger et al., 1999) and calculated the median value from the results of DFA at each channel. DFA is a

method for quantifying the correlation property in a nonstationary time series by computing a scaling exponent using

a modied root mean square analysis of a random walk.

Briey, the analysis is applied to a discrete time series

x(i), i = {1, . . ., N}, which in the present study represents

the synchronization likelihood averaged over all pairs of

channels for each time sample (N = 7680/30 = 256). In

the rst step, the mean is subtracted from this time series

and the time series is integrated

2491

k

X

yk

xi hxi

i1

time series. Next, the de-meaned, integrated time series

y(k) is divided into a number of segments with length n

(n represents the time scale of observation). In this study

we used the following time segment lengths: 0.1, 0.15,

0.2, 0.25, 0.3, 0.35, 0.4, 0.45, 0.5, 0.55 and 0.6 s (equivalently 25, 37, 49, 61, 73, 85, 97, 109, 121, 133 and 145 samples in segment lengths. The above procedure is illustrated

in Fig. 1. The samples are the number of points, which

should be a positive number for the nature of the analysis.

Therefore, the numbers were rounded o). For each of

these segments, the local least-squares linear t is determined. The ensuing piecewise linear t is designated

yn(k). Then, the integrated time series y(k) is detrended

by subtracting the local linear t yn(k) for each segment.

The root mean square uctuation of this integrated and

detrended time series is given by:

r

1 XN

2

F n

yk y n k

k1

N

Fig. 1. Time course of instantaneous amplitude of broad band oscillations. The amplitude at 15 Hz is shown for a typical F3 channel in the depressed

patient and healthy control during 30 s (a and b, respectively). Enlarged segment of time interval 03 s, for the depressed patient and healthy control (c and

d, respectively). For Fig. 2 data are presented for the same subject, F3 channel.

2492

a range of dierent scales n (in the present study n ranged

from 25 samples to 145 samples). In the nal step, the logarithm of F(n) is plotted as a function of the logarithm of

the time scale n (we used logarithms with a base of the

number e). If the time series x(i) has self-similar, scale-free

(fractal) properties, this plot will display a linear scaling

region with a certain scaling exponent. The slope of the line

relating Ln(F(n))/Ln(n) determines the scaling exponent

(self-similarity parameter), which is the result of DFA

(Peng et al., 1995; Goldberger et al., 1999). Fig. 2 shows

an example of DFA for the amplitude envelope of the

broad band oscillations, demonstrating a linear relationship between Ln(n) and Ln(F(n)) in the 030 s range.

The scaling exponent provides a quantitative measure of

LRTC that exist in the EEG. When the EEG is completely

uncorrelated (Gaussian or non-Gaussian probability distribution), the calculation of the scaling exponent yields 0.5,

also called white noise. When applied to the EEG with

LRTC, power-law behavior will generate scaling exponents

with either greater than 0 and less than 0.5 or greater than

0.5 and less than 1. A scaling exponent greater than 0.5 and

less than 1 indicates the data are correlated such that large

uctuations are likely to be followed by large uctuations

and small uctuations are likely to be followed by small

uctuations. The case of scaling exponent = 1 is a special

one which corresponds to 1/f noise, the LRTC became

independent of the time innite range (Bak et al., 1987).

As the scaling exponent increases from 0.5 toward 1, the

LRTC in the EEG are more persistent (decaying more

slowly with time). If a scaling exponent is greater than 1,

the LRTC no longer exhibits power law behavior. Finally,

if the scaling exponent = 1.5, this indicates Brownian noise,

which is the integration of white noise (Peng et al., 2000;

Parish et al., 2004).

controls were carried out using a t-test for the mean values of the scaling exponents of these two conditions. In

addition, a mixed-model repeated-measures ANOVA (2

within and 1 between) was used to determine signicance. The within-group variables are the recording site

(SITE: measured at F3, F4, C3, C4, T3, T4, O1 and

O2) and recording hemisphere (HEMISPHERE: right

and left hemisphere), and the between-group variable is

the participant group (GROUP: depressed patients and

healthy controls). The Greenhouse-Geisser correction

for multiple factors was adopted to control for the

assumption of sphericity. Finally, correlations between

the severity of depression (BDI scores) and the scaling

exponents were determined with Pearson correlation

coecients. All statistical procedures were performed

using SPSS Version 10.0 for Windows. The signicance

level was set at p < 0.05.

In order to test non-linearity in the original EEG signals, we compared the scaling exponents of the original

data with those of the corresponding surrogate data

(Theiler and Rapp, 1996). The surrogate data were generated herein by rst computing the Fourier transforms

of the original signals, randomizing the Fourier phase

while preserving the moduli, and then performing inverse

Fourier transforms (Ivanov et al., 1996). Surrogate data

have amplitude spectra identical to the original signals,

but possible temporal correlations are destroyed. Eleven

surrogate data were generated to match each original

data of depressive patients. The scaling exponents of

DFA are computed for both original data and surrogate

data. The statistical signicance (S) for testing non-linearity is dened by

S jDFA exponentsurr DFA exponentorig j=rDFA exponentsurr

exponent of the surrogate data and r (DFA exponentsurr) its standard deviation, while in the following

the scaling exponent of the original data is labeled

DFA exponentorig. This statistic represents the number

of standard deviations (r) of distance from the DFA

exponent of the original data. It follows a Students t

test distribution with 10 degrees of freedom (tg[1a/2]).

For a = 0.05, critical value of t is 2.228. If the value

of S was larger than 2.228, the original data were considered non-linear.

3. Results

3.1. Dierence between the scaling exponents for depressed

patients and healthy controls

Fig. 2. Detrended uctuation analysis (DFA) quanties correlations in

broad band EEG signals. The scaling exponents are 0.918 and 0.614 for

the depressed patient and healthy control, respectively. Same electrode

location and subject as in Fig. 1.

the scaling exponent at each channel. All of the scaling

exponents in the depressed patients and healthy controls

were greater than 0.5 and less than or equal to 1.0, indicat-

Table 1

The scaling exponents of detrended uctuation analysis of resting EEG in

depressed patients (N = 11) and healthy controls (N = 11)

Channel

F3

F4

C3

C4

T3

T4

O1

O2

*

Depressed patient

Healthy control

Mean

SD

Mean

SD

0.96

0.96

0.87

0.86

0.93

0.98

0.82

0.83

0.16

0.18

0.16

0.16

0.14

0.17

0.17

0.20

0.83

0.86

0.75

0.75

0.80

0.84

0.69

0.73

0.11

0.18

0.10

0.09

0.11

0.11

0.10

0.14

t

2.25*

1.29

2.22*

1.95

2.39*

2.36*

2.19*

1.34

Table 2

The scaling exponents of detrended uctuation analysis of resting EEG in

depressed patients (N = 11) and surrogate data (N = 11)

Channel

F3

F4

C3

C4

T3

T4

O1

O2

**

Table 3

Repeated measures ANOVA table for HEMISPHERE main eect

Channel

a

Right hemisphere

Left hemisphereb

Source

SS

DF

MS

ERROR

SITE

0.64

0.31

60

3

.01

.10

9.75

0.001*

ERROR

SITE

0.19

0.24

50.30

2.52

.004

.095

24.97

0.001*

Left hemisphere: sphericity violated, Greenhouse-Geisser corrections

to the D.F. were used to adjust for violations of the sphericity assumption

for repeated measures factors.

*

p < 0.01.

b

p < 0.05.

scaling exponents of depressed patients have relatively

higher values in whole brain regions compared to healthy

controls, with signicant dierences at F3, C3, T3, T4

and O1 channels.

The mean and the standard deviation of the scaling

exponent for depressed patients and surrogate data is

also given in Table 2. The scaling exponents of surrogate

data have signicantly higher values compared with

depressed patients at all channels. The demonstration

of a statistically signicant dierence in scaling exponents

between the original and surrogate data is in keeping

with the presence of non-linear dynamics in the original

signal.

In order to answer the question of whether there is a

global dierence in LRTC between depressed patients

and healthy controls or not, repeated measures ANOVA

was performed for two groups (GROUP: depressed

patients and healthy controls) eight channels (SITE:

measured at F3, F4, C3, C4, T3, T4, O1 and O2). In

the analysis, with F values representing the main eect

of the group (F(1, 20) = 5.15, p < 0.05) and site

(F(7, 140) = 12.33, p < 0.01), the global null hypothesis

that there is no dierence between depressed patients

and healthy controls was rejected. Nevertheless, there

was no signicant interaction of group and site

(F(7, 140) = 0.25, p > 0.05). This suggests that the global

2493

p < 0.05.

p < 0.01.

Depressed patient

Surrogate data

Mean

SD

Mean

SD

0.96

0.96

0.87

0.86

0.93

0.98

0.82

0.83

0.16

0.18

0.16

0.16

0.14

0.17

0.17

0.20

1.08

1.06

1.01

0.99

1.06

1.13

0.93

0.92

0.25

0.23

0.25

0.24

0.19

0.21

0.23

0.21

healthy controls reects the neuronal dynamics related

to generation of depression rather than an incidental

result of the interaction of the group and site.

Next, in order to test inter-hemispheric dierences,

repeated measures ANOVA of LRTC was performed for

two groups (patients and controls) two hemispheres

(F3, C3, T3 and O1 classied as left hemisphere and F4,

C4, T4 and O2 as right). The right hemisphere satised

the sphericity assumption but the left hemisphere violated

this assumption. Thus, a Greenhouse-Geisser correction

was performed in the left hemisphere. A signicant main

eect was observed for both hemispheres (Table 3). Additionally, repeated measures ANOVA was performed for

two groups (patients and controls), considering four channels at each hemisphere. The ANOVA of LRTC yielded a

signicant main eect of the group in the left hemisphere,

F(1, 20) = 5.87, p = 0.025, but a marginal trend in the right

hemisphere, F(1, 20) = 4.14, p = 0.055 (Table 4). This suggests a better discrimination between depressed patients

and healthy controls for the left hemisphere than for the

right.

3.2. Correlations between the BDI and scaling exponents

Finally, to determine the possible eect of severity of

depression on the scaling exponents, the correlations

between the scaling exponents and the BDI score of the

participants were examined. Fig. 3 shows the correlations

between the scaling exponents and the BDI score of the

participants. The BDI score was signicantly correlated

with the scaling exponents at F3, F4, C3, C4, T3, T4 and

O1.

t

3.08*

2.83*

3.83*

2.76*

3.79**

3.79**

2.26*

2.97*

Table 4

Repeated measures ANOVA table for GROUP main eect

Channel

Source

SS

DF

MS

ERROR

GROUP

1.26

0.37

20

1

0.06

0.37

5.87

0.025*

ERROR

GROUP

1.32

0.27

20

1

0.07

0.27

4.14

0.055

*

p < 0.05.

2494

Fig. 3. Correlations between the DFA power-law scaling exponents of resting EEG and severity of depression of total participants (N = 22). BDI, Beck

depression inventory; *p < 0.05, **p < 0.01.

4. Discussion

In this study we analyzed the resting EEG of 11 unmedicated depressed patients and 11 healthy control participants by means of DFA, a scaling analysis method that

quanties a simple parameter to represent the correlation

properties of a time series. The scaling exponent, the result

of DFA, provides a quantitative measure of LRTC that

exists in the EEG. The present study demonstrates that

all the scaling exponents in depressed patients and healthy

controls were greater than 0.5 and less than 1.0, regardless

of their condition. These results show that the broadband

EEG in both depressed patients and healthy controls exhibit LRTC with power-law behavior.

Several studies have applied DFA to broadband EEG

and have found indications of LRTC with power-law

behavior. Watters and Martin (2004) reported that a mean

scaling exponent of 0.67 was the result of DFA applied to

the EEG obtained from 3 to 100 Hz, and our previous

study (Lee et al., 2007) reported a score of 0.91 from psychiatric outpatients. The main reasons for this dierence

are presumed to be that all of the participants of the latter

study had psychopathologies and were not controlled by

psychiatric medications. In this study, the mean scaling

exponent across all participants and sites of EEG was

0.84, which is located between the result of Watters and

Martin (2004) and the result obtained by our previous

study.

For the EEG data, non-linear dynamics algorithms can

give spurious results. Recently, the surrogate data techniques have been developed to distinguish the non-linear

systems from the linearly correlated noise (Theiler and

Rapp, 1996). We found that the scaling exponents of surrogate data have signicantly higher values compared with

depressed patients at all channels. That is a strong indication of the non-linear structure in the original EEG data.

From the above, it is apparent that LRTC with powerlaw scaling is a fundamental feature of brain activity. Further, the presence of power-law scaling behavior in the

temporal correlations with large (small) uctuations that

tend to cluster together in time, as seen in other complex

systems exhibiting power-law scaling behavior (Peng

et al., 1995).

Furthermore, we found that depressed patients demonstrate higher values of the scaling exponents at all channels

than healthy control participants, with signicant dierences detected at F3, C3, T3, T4 and O1 channels. This

result suggests that the EEG oscillations exhibit more persistent tendency of the LRTC in depressive patients compared to healthy controls. Although this dierence does

not implicate a specic underlying mechanism of depression, it suggests that distinct mechanisms underlie the

EEG oscillations. It could be that the mechanism responsible for higher values of the scaling exponents in depressed

patients than healthy controls is responsible for the psychophysiological changes seen in depression.

In this study, the mean scaling exponent of depressed

patients was 0.90 and the value of healthy controls was

0.78. In a previous study that analyzed broadband EEG,

Parish et al. (2004) reported that the scaling exponent of

the epileptogenic hippocampus was 0.680.88 as a result

of DFA applied to intracranial EEG data of the hippocampal area for 5 patients with a unilateral mesial temporal

lobe seizure. On the other hand, it was between 0.60 and

0.69 in the non-epileptogenic hippocampus. In the study

of DFA applied to sleep apnea patients, Lee et al. (2004)

also reported that the scaling exponent increased as sleep

became deeper in that it was 0.95, 1.00, 1.12, 1.22 in waking, stage 1, stage 2, and stage 34 sleep, respectively.

Recently Gifani et al. (2007) applied DFA to EEG to measure the depth of anesthesia and reported that the scaling

exponent was increased from 0.8 to 2 as it changed from

awake to moderate and then deep anesthesia. Connected

to this point, a signicant dierence was found only in

the upper alpha band (1013 Hz) as a result of DFA in Alzheimer disease (AD) patients and non-demented participants with subjective memory complaints (SC). The

greater than 0.786 of the SC group (Stam et al., 2005).

The pathophysiological implications of slower decay of

the LRTC in the EEG in depression, dementia, and deeper

anesthesia/sleep are not clear. However, major depression,

Alzheimer dementia, anesthesia and sleep are commonly

accompanied by the decline of cognitive function. On the

other hand, cognitive abilities are increasingly linked to

the dynamics of neuronal oscillations on many spatial

scales and at various frequencies (Varela et al., 2001; Buzsaki and Draguhn, 2004). These ndings suggest that the

persistence of LRTC in the EEG is closely related to cognitive ability. Thus, one can speculate that in the case of

depression, slow decay is related to the reduction of cognitive abilities in depressive disorder, such as ruminations

and psychomotor retardation (Widlocher, 1983).

As previously mentioned, the scaling exponent of

depressed patients was signicantly higher than healthy

controls at F3, C3, T3, T4 and O1 channels. Furthermore,

there was no systemic variation across recording channels

for these dierent groups shown only in the left hemisphere. Therefore, our results indicated that depressed

patients have signicantly higher values of the scaling

exponents over the left hemisphere and both temporal

regions than healthy controls.

In 1996, Sheline et al. demonstrated a signicant inverse

correlation between depression and left hippocampal volume. Vakili et al. (2000) also found that left hippocampal

volumes correlated with the HDRS. Using PET, subsequent studies showed that the amount of depletion of serotonin (S2) receptors in the left temporal cortex was

signicantly correlated with the severity of depressive

symptoms (Mayberg et al., 1988). On the other hand, some

investigators have suggested that a left hemispheric epileptic focus may be a factor predisposing to depression (Septien et al., 1993; Altshuler et al., 1990). Thus, the results of

our study are in line with previous studies showing depressive episodes have been associated with temporal structures

(Sheline et al., 1996; Vakili et al., 2000; Mayberg et al.,

1988) and left hemispheric structures (Septien et al., 1993;

Altshuler et al., 1990).

To gain further insights into the basis for the LRTC in

the EEG and major depressive disorder, we tested whether

the scaling exponent was related to the severity of depression in the participants. A signicant linear correlation

was observed between the score in the BDI and the scaling

exponent over most of the channels, except O2. In other

words, a brain aected by major depressive disorder shows

slower decay of the LRTC and the persistence of the LRTC

of EEG in depressed patients was associated with the severity of depression over most of the cortical areas.

This study suggests that further clarication would show

how the DFA method can broaden our understanding of

the psychophysiological basis of depression. Future studies

should focus on researching of the slower decay of LRTC

of EEG changes with the recovery from a depressive episode. Future works should also include the comparison

2495

other neuroimaging methods.

Acknowledgement

This work was supported by the Korea Research Foundation Grant funded by the Korean Government (KRF2006-E00071).

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