European Psychiatry 27 (2012) 245249

Original article

Temperament proles, major depression, and response to treatment with SSRIs

in psychiatric outpatients
O. Kampman a,*,d, O. Poutanen a,b, A. Illi a, E. Setala-Soikkeli c, M. Viikki a,e, T. Nuolivirta d, E. Leinonen a,b
a

University of Tampere, Medical School, 33014 Tampere, Finland

Tampere University Hospital, Department of Psychiatry, 33014 Tampere, Finland
c
Kanta-Hame Central Hospital, Department of Psychiatry, Hameenlinna, Finland
d
Seinajoki Hospital District, Department of Psychiatry, Seinajoki, Finland
e
Tampere Mental Health Centre, Tampere, Finland
b

A R T I C L E I N F O

A B S T R A C T

Article history:
Received 1 April 2010
Received in revised form 14 July 2010
Accepted 14 July 2010
Available online 8 October 2010

Objective: The Temperament and Character Inventory (TCI) is commonly used in adult populations. Our
aim was to explore: (1) if there are specic differences in temperament dimensions related to depression
in comparison with general population, (2) if the treatment response during the acute phase of major
depressive disorder (MDD) is predictable by TCI temperament dimensions.
Method: Temperament proles in 98 MDD patients were compared with a Finnish community sample.
The patients were treated with serotonin selective reuptake inhibitors (SSRIs) for 6 weeks and their
temperament proles were assessed at baseline and endpoint. The harm avoidance (HA) and depression
scores at baseline and endpoint were modelled with path analysis. For path modelling, we tested the
relationships between different temperament dimensions and depression symptoms and other clinical
variables with Mancova model.
Results: The HA scores were signicantly higher in patients both at baseline and endpoint compared to
the Northern Finland 1966 Birth Cohort (NFBC). The patients, and especially males, had slightly higher
reward dependency (RD) scores. HA at endpoint explained moderately the Montgomery Asberg
Depression Rating Scale (MADRS) endpoint score. HA endpoint score was strongly explained by HA
baseline score.
Conclusions: HA is associated with risk of and treatment response to depression.
2010 Elsevier Masson SAS. All rights reserved.

Keywords:
Temperament
Inventories
Major depression
Antidepressive agents
Second generation
Therapeutic use

1. Introduction
The association between temperament and depression is
complex. There seem to be potentially four types of relationships
at least between harm avoidance (HA) temperament dimension
and depression: a) inuence of state on trait measure, b) HA as a
susceptibility factor for depression, c) elevated HA scores even
after remission of acute depressive symptoms, and d) a pathoplastic effect of HA on the expression of depression [21].
Behavioural inhibition has been described as one of the
temperament dimensions in the psychobiological model by
Cloninger et al. [5]. The temperament dimensions in this model
have been dened as individual differences in associative learning
in response to novelty, danger or punishment, and reward.
Cloningers et al. model of temperament is based on genetic
studies of personality in humans and neurobiological studies with

The work was done in Tampere Mental Health Care Centre and Kanta-Hame
Central Hospital, Department of Psychiatry.
* Corresponding author.Tel.: +358 44 4155547(mobile); fax: +358 3 35516164.
E-mail address: olli.kampman@uta. (O. Kampman).

0924-9338/$ see front matter 2010 Elsevier Masson SAS. All rights reserved.
doi:10.1016/j.eurpsy.2010.07.006

rodents. Temperament dimensions in the model have been

hypothesized to be related to the neurotransmitter systems of
the brain [5,15,20].
Specic temperament inventories are used in assessing
behavioural inhibition and other temperament dimensions. The
Temperament and Character Inventory (TCI) is one of the most
widely used scales in adult populations [5]. The TCI includes four
dimensions of temperament: 1) novelty seeking (NS) with its
facets exploratory excitability, impulsiveness, extravagance, disorderliness, 2) HA with its facets anticipatory worry, fear of
uncertainty, shyness with strangers, fatigability, 3) reward
dependence (RD) and its facets sentimentality, attachment,
dependence, and 4) persistence (P) without any facets, and three
dimensions of character: self-directedness (SD), cooperativeness
(CO), and self-transcendence (ST) [5].
Cultural issues may cause variation when assessing dimensions
of temperament or character [10]. In Finland, the psychometric
properties of the TCI have been evaluated in a large 31-year-old
general population [16]. In subsequent comparison with an
American cohort, the Finnish cohort had higher mean scores in
NS and HA whereas in RD and P, the American sample had higher

246

O. Kampman et al. / European Psychiatry 27 (2012) 245249

scores. In the Finnish cohort, the female subjects had higher values
of the HA and the RD subscales compared with males [17].
Mulder [19] identied seven studies on treatment outcome in
depression using a former version of TCI, the Tridimensional
Personality Questionnaire (TPQ) [6], as temperament measure.
According to this review, four of these studies failed to show any
association between HA score and treatment outcome, whereas in
two of the studies, high HA was associated with poor outcome. In
four case-control studies using TCI, the change in HA score was
positively correlated with recovery from depression [3,13,22,23].
The aims of the present study were to explore 1) if there are
specic differences in temperament dimensions related to
depression compared to a general population sample (statedependent personality change and/or personality trait as a
susceptibility factor), 2) if there are specic differences in
temperament dimensions related to patients who respond to
treatment as opposed to patients who do not respond to treatment
(state-dependent personality change and/or personality trait as a
pathoplastic factor), 3) how is treatment response during the acute
phase of major depressive disorder (MDD) predicted by baseline
HA temperament dimension together with depression severity
(personality characteristic as a pathoplastic factor), and 4) how is
post-treatment HA temperament dimension predicted by baseline
HA and depression severity (personality change induced by
preceding depression severity after remission of depression
[scar].
2. Material and methods
The study population comprised 98 individuals 19 to 72 years of
age (41 males and 57 females, age mean [S.D.] 40.5 [14.1] years),
who were patients in secondary outpatient services in the city of
Tampere or the Kanta-Hame Hospital District, Finland (total
catchment population approximately 300,000). The patients were
recruited for a pharmacogenetic study on depression during the
time period from September 2002 to December 2006 (the DEPGEN
Study).
All patients fullled the following criteria on entrance to the
study: 1) current episode of MDD according to DSM-IV-criteria, 2) a
Montgomery Asberg Depression Rating Scale (MADRS) [18] score
of at least 20. MADRS is a 10-item diagnostic interviewer rating
questionnaire intended to measure the severity of depressive
episodes and designed especially to be sensitive to changes due to
antidepressants and other forms of treatment. We considered a
rating scale of interviews by trained psychiatrists to be a more
valid choice than a self-report instrument. MADRS seems to be
superior to the Hamilton Depression Scale (HAM-D) in clinical
trials [2]. A score of at least 20 was used as an entrance level in
order to distinguish between moderate and mild depression [25].
Patients with somatic diseases causing depression were excluded, likewise patients with bipolar disorder, schizophrenia, severe
personality disorders or substance-related disorders. Patients who
had been prescribed antidepressive medications during the past
3 months, or who were currently taking mood stabilizing or
antipsychotic medications were also excluded. Eighteen of the
patients had an earlier diagnosed depressive episode. All other
patients were having their rst depressive episode.
The clinical researchers conducted a screening interview with
each patient either by telephone or face-to-face before the initial
assessment for the study. The patients completed the 107 temperament items from the 240-item TCI questionnaire (version 9) at the
initial assessment and after 6 weeks of follow-up. MADRS interviews were conducted simultaneously. The character dimensions
of the TCI were not used in the study as the primary focus was
pharmacogenetic. All patients were prescribed SSRIs, either
citalopram, uoxetine or paroxetine (the three most-prescribed

SSRIs in Finland at the time of the study). The dosage of the

medication was adjusted according to the clinical response, which
was checked after 3 weeks during a short study visit. The nal
medication response was determined as at least 50% reduction in
the MADRS score during follow-up. Medication adherence was
self-monitored by keeping a paper-and-pencil medication diary. At
least, 80% adherence rate was considered to be adequate
treatment. Anxiolytics and hypnotics in minor doses were allowed
as concomitant medications at the early stage of the treatment
period. The researchers, who were all experienced psychiatrists,
were responsible for medical treatment during follow-up. All
patients gave written informed consent and the local ethics
committee approved the study protocol.
The general population sample used as an historical control
population for the patients comprised 4349 subjects (1974 males,
2375 females) representing a part of the Northern Finland 1966
Birth Cohort (NFBC 1966). The results of the TCI temperament
questionnaire studied at 31-year follow-up within this cohort have
been reported by Miettunen et al. [16] together with a
psychometric analysis of the TPQ and TCI temperament scales.
The article also includes a detailed description of the NFBC 1996
sample [16].
3. Statistical methods
We compared temperament distributions between the depressive patients and the NFBC 1966 population, and modelled the
relationships between HA temperament dimension and course of
acute symptoms of depression during treatment with SSRIs. The
comparisons of means for baseline and endpoint TCI temperament
dimensions (NS, HA, RD and P) between DEPGEN patients and the
NFBC 1966 cohort were analysed with Students t tests for
independent samples. The calculations were made for total
samples and for men and women separately to analyse the
differences between patient sample and the general population
sample. Comparisons of means on baseline and endpoint TCI
temperament dimensions (NS, HA, RD and P) were also made in the
patient population between responders and nonresponders with
Students t test for independent samples.
The relationships between MADRS and HA baseline and
endpoint scores were analysed by the path analysis method. The
path analysis method is mathematically equivalent to multiple
regression analysis, but this method makes it possible to explore
different causalities between variables and to describe them
graphically including covariance coefcients between selected
variables. For path modelling, we tested the relationships between
different temperament dimensions and depression symptoms and
other clinical variables with multiple analysis of covariance
(MANCOVA) model. In this model, the endpoint temperament
dimensions were used as target variables and age, gender, previous
depressive episode, and baseline (pretreatment) and endpoint
(post-treatment) depression score as explanatory variables. In the
path model, the baseline variables were added as independent (xvariables) and endpoint variables as dependent (y-variables). The
proportions of explained variance in the structural equation
models are indicated as blocked-error R square (beR2) values. All
other calculations were made with SPSS (version 17.0), except that
the comparisons between DEPGEN and NFBC 1966 temperament
means were analysed with GraphPad QuickCalcs software
(www.graphpad.com). The path analysis modelling was made
with LISREL for Windows (version 8.80).
4. Results
Eighty-seven patients completed the study (both MADRS and
TCI assessments after 6 weeks) and in addition, one patient

O. Kampman et al. / European Psychiatry 27 (2012) 245249

completed TCI after 6 weeks. Of the 87 patients, 51 were

responders and 36 nonresponders. Thirty (34.5%) of the patients
were in remission after 6 weeks treatment (MADRS score 7 or
less). In comparisons of means of baseline and endpoint, TCI
temperament dimensions (NS, HA, RD and P) between DEPGEN
patients and the NFBC 1966 cohort the HA mean scores were
signicantly higher in patients both at baseline and endpoint
compared to the NFBC 1966 cohort (HA-baseline & endpoint total,
men and women, t = 9.015.2 in different groups, P < 0.001
between all groups). The NS score means did not differ between
the total samples, men or women (NS-baseline total, t = 1.15,
P = 0.25; NS-baseline men, t = 0.53, P = 0.59; NS-baseline women,
t = 1.26, P = 0.21; NS-endpoint total, t = 0.94, P = 0.35; NS-endpoint
men, t = 0.80, P = 0.42; NS-endpoint women, t = 0.36, P = 0.72; t
test). The patients had slightly higher RD score means, which was
explained by the difference in the males group (RD-baseline total,
t = 2.1, P = 0.04; RD-baseline men, t = 1.9, P = 0.06; RD-baseline
women, t = 1.1, P = 0.27; RD-endpoint total, t = 3.2, P = 0.002; RDendpoint men, t = 2.7, P = 0.006; RD-endpoint women, t = 0.8,
P = 0.16). The P score means did not otherwise differ between the
patients and NFBC 1966 cohort, but female patients had higher
means at baseline (P-baseline total, t = 0.59, P = 0.52; P-baseline
men, t = 1.1, P = 0.27; P-baseline women, t = 2.2, P = 0.03; Pendpoint total, t = 0.5, P = 0.61; P-endpoint men, t = 0.3, P = 0.73;
P-endpoint women, t = 0.8, P = 0.41). The means and S.D. for all
temperament dimensions for patients and cohorts are shown in
Table 1.
The patient group was 10 years older on average than the NFBC
1966 group. Therefore, we also analysed correlations between age
and temperament dimensions in the patient population. Correlations were signicant between age and NS baseline (r =
0.30,
P = 0.03), NS endpoint (r =
0.34, P = 0.01), and RD endpoint scores
(r =
0.21, P = 0.04). All other correlations were nonsignicant.
In comparisons of temperament dimensions within the patient
group, HA scores were lower and NS and P scores higher in the
responders group than in the nonresponders group both at
baseline and endpoint (Table 2).

247

Fig. 1. Path analysis chart between Montgomery Asberg Depression Rating Scale
and harm avoidance baseline and endpoint scores in the DEPGEN study. Chart
gures indicate estimates of regression coefcients between variables.
MADRS endpoint = 0.71*HA endpoint (Z = 5.32, P = 0.000) + 0.83*MADRS baseline
(Z =
1.95, P = 0.052) 0.29*HA baseline (Z = 6.96, P = 0.000); beR2 = 0.48 or
MADRS endpoint = 0.82*MADRS baseline (Z = 5.00, P = 0.000) + 0.36*HA baseline
(Z = 3.69, P = 0.000); beR2 = 0.32 (reduced model).
HA endpoint =
0.013*MADRS baseline (Z =
0.11, P = 0.9) + 0.92*HA baseline
(Z = 6.96, P = 0.000); beR2 = 0.68.

In the MANCOVA model, HA appeared to be accounted for a

greater explanatory proportion than the other three temperament
dimensions together (adjusted R squares with the complete model
for HA = 0.26, NS = 0.11, RD = 0.06 and P = 0.02, and with MADRS
endpoint score for HA = 0.26, NS = 0.05, RD = 0.01 and P = 0.09)
indicating the crucial role of HA in treatment response. The path
analysis model estimates between MADRS and HA baseline and
endpoint scores were as follows (Fig. 1).
5. Discussion
As cultural differences have been found in the distributions of
temperament dimensions [17], it was important to use a Finnish
cohort as a control population. The DEPGEN population showed, as
expected, high HA score at both baseline and endpoint compared
to the NFBC 1966 cohort. Our result is consistent with earlier
studies using TCI as a temperament measure [13,22,23]. We also

Table 1
Means and standard deviations of temperament dimensions in DEPGEN patients at baseline and after 6 weeks of antidepressive treatment and among NFBC 1996 cohort
subjects (Miettunen et al. 2004, [16]).
Patients baseline mean (S.D.)
Temperament dimension

Novelty seeking
Harm avoidance
Reward dependency
Persistence
a
b
c
d
e

Patients endpoint mean (S.D.)

NFBC 1966 cohort mean (S.D.) [16]

Men

Women

All

Men

Women

All

Men

Women

All

n = 41

n = 57

n = 98

n = 36

n = 52

n = 88

n = 1974

n = 2375

n = 4349

19.2 (7.4)
22.6 (6.6)a
14.3 (3.9)
4.2 (2.0)

19.8 (7.6)
24.4 (7.1)a
16.5 (3.7)
4.6 (2.1)e

19.6 (7.5)
23.6 (6.9)a
15.5 (3.9)c
4.4 (2.1)

20.5 (7.3)
20.8 (8.2)a
14.9 (3.7)b
4.4 (1.7)

21.1 (7.5)
22.5 (7.7)a
16.7 (3.6)
4.3 (2.3)

20.9 (7.4)
21.8 (7.9)a
16.0 (3.7)d
4.4 (2.1)

19.7 (5.9)
13.0 (6.2)
13.2 (3.7)
4.5 (1.7)

20.8 (5.9)
14.9 (6.0)
16.0 (3.4)
4.1 (1.7)

20.3 (5.9)
14.1 (6.1)
14.7 (3.8)
4.3 (1.8)

t = 9.015.2 in different groups, P < 0.001 compared with Northern Finland 1966 Birth Cohort subjects in all groups (men, women, all).
t = 2.7, P = 0.006 compared with men in Northern Finland 1966 Birth Cohort.
t = 2.1, P = 0.04 compared with total Northern Finland 1966 Birth Cohort.
t = 3.2, P = 0.002 compared with total Northern Finland 1966 Birth Cohort.
t = 2.2, P = 0.03 compared with women in Northern Finland 1966 Birth Cohort.

Table 2
Temperament scores in 87 patients grouped according to their response to SSRI medications during 6 weeks treatment for major depression. Response determined as at least
50% reduction in Montgomery Asberg Depression Rating Scale score. All statistics are comparisons between responders and nonresponders.
Temperament dimension

Responders n = 51

Nonresponders n = 36

t test value, signicance

Novelty seeking baseline

Novelty seeking endpoint
Harm avoidance baseline
Harm avoidance endpoint
Reward dependency baseline
Reward dependency endpoint
Persistence baseline
Persistence endpoint

21.4 (7.2)
22.8 (7.2)
22.1 (6.3)
19.3 (7.9)
15.7 (3.8)
16.1 (3.4)
4.8 (1.9)
4.8 (1.9)

16.9 (7.9)
17.8 (6.7)
26.6 (6.9)
25.8 (6.1)
15.1 (4.3)
15.6 (4.0)
3.9 (2.2)
3.6 (2.1)

t = 2.7, P = 0.009
t = 3.3, P = 0.002
t = 3.2, P = 0.002
t = 4.1, P < 0.001
t = 0.60, P = 0.55
t = 0.70, P = 0.49
t = 2.1, P = 0.04
t = 2.8, P = 0.007

248

O. Kampman et al. / European Psychiatry 27 (2012) 245249

obtained a slightly higher RD score for the total patient sample at

baseline and for men at endpoint. The result concerning RD is
contradictory to some earlier ndings within general population,
according to which high RD may protect against depression [4,11].
However, in the study by Richter et al. [22], the RD score was
slightly higher among MDD patients than among controls. Our
nding may also be in line with the ndings of Elovainio et al. [9], in
which one facet of RD sentimentality was positively associated
with future depression. The variation in these ndings may
indicate that the meaning of RD as a vulnerability factor is limited,
and may be related to the selection of study populations. It is also
possible that the lower factor validity of RD compared with NS or
HA in the 9th version of the TCI biased the results in this respect, as
was found in the study by Kose et al. [14]. In the studies by
Miettunen et al. 2004 [16] and Gutierrez et al. 2001 [12],
sentimentality was found to be different from other RD facets
(attachment, dependence). Although the patient population was
older on average than the NFBC 1966 cohort, this age difference did
not affect the results, as signicant correlations between age and
temperament dimensions NS and RD were all negative. However,
the endpoint NS scores were on the same level in patients and in
controls, which could have resulted in a signicant difference in
comparison with an older control population [17].
The comparisons within patient population between responders and non-responders were in line with some earlier studies
where higher HA score was associated with poorer treatment
response in depression [1,7,8,13]. Corresponding analyses with
other temperament dimensions (NS, RD and P) have resulted in
heterogeneous results in these studies, which is likely related to
different study methodology, including patient selection, sample
size, type of treatment and follow-up time. The differences in NS
and P scores in our study in the opposite direction than with HA
can be regarded as clinically meaningful ndings associated with
depression. Also in the Mancova model, the most marked
explaining proportion between treatment related variables and
HA was found, compared with NS and P.
The analyses of the course of depressive symptoms in relation
to the temperament dimensions were performed to enhance our
knowledge for future pharmacogenetic studies on depression, and
also for a better understanding of the impact of biological factors
on recovery from major depression. We performed a path analysis
on the relationships between the course of depressive symptoms
during the acute phase of treatment and HA levels before and after
treatment with SSRIs. This analysis showed that high HA is
relatively stable during acute treatment phase, and was not
associated with the severity of major depression. However, a
moderate positive relationship between HA and treatment
outcome of depression was apparent. Only the temperament
dimensions of the TCI were involved in our study, not the character
dimensions. HA and the character dimension of SD seem to be
negatively correlated [13,24]. Thus the relationships described
here to increased HA could also be due to decreased SD.
The model explained moderate to high proportions of variations
for both outcome variables. Of the four potential types of relationships between HA and depression (a, b, c and d in the introduction to
this paper) described by Pelissolo and Corruble [21] type b could be
found. However, a main limitation in the study design is the lack of
age- and gender-matched control population corresponding in
numbers with the patient group. The results of comparisons with the
NFBC 1966 population must be interpreted with caution due to the
markedly different age distribution of the control sample. Therefore,
the role of this nding as an evidence of a state-dependent
personality change or a pathoplastic factor for SSRI response cannot
be conclusively determined. Considering the named limitations, the
results support earlier ndings on the role of HA as a vulnerability
factor for depression. An interesting nding in the path analysis was

the moderately negative relation between baseline HA and posttreatment symptoms when taking into account the endpoint HA
despite strong positive relations between HA ratings and posttreatment symptoms, as well as between endpoint HA and posttreatment symptoms. It is possible that this nding is due to
individual variation in the change of HA during treatment. For
example, in some patients, a high state-related increase of HA during
depression could predict a good treatment response.
Other methodological limitations of the study include the
restricted 6 weeks follow-up time and the exclusion of the
character dimensions of the TCI. Long-term studies with larger
numbers of recurrent patients are needed for a better test of the
scar hypothesis. It is notable that by using scale variables in the
path analysis and performing the analysis for responders and
nonresponders together, we cannot exclude the possibility that
each subcategory could have a specic type of relationship
between temperament and outcome after 6 weeks. The relationship found between depression severity at endpoint and HA at
endpoint may indicate support for 1) HA as a pathoplastic factor for
depression severity at endpoint, and/or 2) HA as a state-dependent
change of personality at endpoint. In the path analysis, the
correlations between two or more variables may not represent
direct causality between the factors, as there could be unexplained
variance due to variables not included in the analyses.
In conclusion, the HA temperament dimension is obviously
associated with both the occurrence of depressive symptoms and
treatment response in major depression. There is also some
evidence supporting high HA indicating susceptibility to depression, but more longitudinal studies are needed to conrm this
nding. The nding concerning RD implies a need for further
studies with larger populations and with TCI including all its facets.
Role of funding source
The DEPGEN study was funded by grants from Pirkanmaa and
Kanta-Hame Hospital Districts. Dr. Kampman received a research
grant from The Finnish Medical Foundation. Dr. Illi received
research grants from H. Lundbeck/Finland and Lilly Foundation/
Finland. None of the funding sources had any further role in study
design, in the collection, analysis and interpretation of data, in the
writing of the report or in the decision to submit the paper for
publication.
Conict of interest
All the authors conrm that they have no conict of interest for
the submitted study.
References
[1] Agosti V, McGrath PJ. Comparison of the effects of uoxetine, imipramine and
placebo on personality in atypical depression. J Affect Disord 2002;71:11320.
[2] Carmody TJ, Rush AJ, Bernstein I, Warden D, Brannan S, Burnham D, et al. The
Montgomery Asberg and the Hamilton ratings of depression: a comparison of
measures. Eur Neuropsychopharmacol 2006;16:60111.
[3] Celikel FC, Kose S, Cumurcu BE, Erkorkmaz U, Sayar K, Borckardt JJ, et al.
Cloningers temperament and character dimensions of personality in patients
with major depressive disorder. Compr Psychiatry 2009;50:55661.
[4] Cloninger CR, Bayon C, Svrakic DM. Measurement of temperament and character in mood disorders: a model of fundamental states as personality types. J
Affect Disord 1998;51:2132.
[5] Cloninger CR, Svrakic DM, Przybeck TR. A psychobiological model of temperament and character. Arch Gen Psychiatry 1993;50:97590.
[6] Cloninger CR, Przybeck TR, Svrakic DM. The tridimensional personality questionnaire: US normative data. Psychol Rep 1991;69:104757.
[7] Corruble E, Duret C, Pelissolo A, Falissard B, Guel JD. Early and delayed
personality changes associated with depression recovery? A one-year follow-up study. Psychiatry Res 2002;109:1725.
[8] de Winter RFP, Wolterbeek R, Spinhoven P, Zitman FG, Goekoop JG. Character
and temperament in major depressive disorder and a highly anxious-retarded
subtype derived from melancholia. Compr Psychiatry 2007;48:42635.

O. Kampman et al. / European Psychiatry 27 (2012) 245249

[9] Elovainio M, Kivimaki M, Puttonen S, Heponiemi T, Pulkki L, KeltikangasJarvinen L. Temperament and depressive symptoms: a population-based
longitudinal study on Cloningers psychobiological temperament model. J
Affect Disord 2004;83:22732.
[10] Farmer A, Mahmood A, Redman K, Harris T, Sadler S, McGufn P. A sib-pair
study of the Temperament and Character Inventory scales in major depression. Arch Gen Psychiatry 2003;60:4906.
[11] Grucza RA, Przybeck TR, Spitznagel EL, Cloninger CR. Personality and depressive symptoms: a multidimensional analysis. J Affect Disord 2003;74:12330.
[12] Gutierrez F, Torrens M, Boget T, Martin-Santos R, Sangorrin J, Perez G, et al.
Psychometric properties of the Temperament and Character Inventory (TCI)
questionnaire in a Spanish psychiatric population. Acta Psychiatr Scand 2001;
103:1437.
[13] Hirano S, Sato T, Narita T, Kusunoki K, Ozaki N, Kimura S, et al. Evaluating the
state dependency of the Temperament and Character Inventory dimensions in
patients with major depression: a methodological contribution. J Affect Disord
2002;69:318.
[14] Kose S, Sayar K, Kalelioglu U, Aydin N, Celikel FC, Gulec H, et al. Normative data
and factorial structure of the Turkish version of the Temperament and
Character Inventory. Compr Psychiatry 2009;50:3618.
[15] Menza MA, Forman NE, Goldstein HS, Golbe LI. Parkinsons disease, personality, and dopamine. J Neuropsychiatry Clin Neurosci 1990;2:2827.
[16] Miettunen J, Kantojarvi L, Ekelund J, Veijola J, Karvonen JT, Peltonen L, et al. A
large population cohort provides normative data for investigation of temperament. Acta Psychiatr Scand 2004;110:1507.

249

[17] Miettunen J, Veijola J, Lauronen E, Kantojarvi L, Joukamaa M. Sex differences in

Cloningers temperament dimensions a meta-analysis. Compr Psychiatry
2007;48:1619.
[18] Montgomery SA, Asberg M. A new depression scale designed to be sensitive to
change. Br J Psychiatry 1979;134:3829.
[19] Mulder RT. Personality pathology and treatment outcome in major depression: a review. Am J Psychiatry 2002;159:35971.
[20] Peirson AR, Heuchert JW, Thomala L, Berk M, Plein H, Cloninger CR. Relationship between serotonin and the temperament and character inventory. Psychiatry Res 1999;89:2937.
[21] Pelissolo A, Corruble E. Personality factors in depressive disorders: contribution of the psychobiologic model developed by Cloninger. Encephale 2002;
28:36373.
[22] Richter J, Eisemann M, Richter G. Temperament and character during the
course of unipolar depression among inpatients. Eur Arch Psychiatry Clin
Neurosci 2000;250:407.
[23] Sato T, Narita T, Hirano S, Kusunoki K, Sakado K, Uehara T. Is interpersonal
sensitivity specic to non-melancholic depressions? J Affect Disord 2001;64:
13344.
[24] Smith DJ, Duffy L, Stewart ME, Muir WJ, Blackwood DH. High harm avoidance
and low self-directedness in euthymic young adults with recurrent, earlyonset depression. J Affect Disord 2005;87:839.
[25] Snaith RP, Harrop FM, Newby DA, Teale C. Grade scores of the Montgomery
Asberg Depression and the Clinical Anxiety Scales. Br J Psychiatry 1986;
148:599601.