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Acta Neu ropsych iatri ca 200 2: 14: 66–70 Copyright CActa Neuropsy chiatrica 2 002
Printed in Denmark. All rights reserved ISSN 0924-2708
Serotonin, personality and borderline
personality disorder
Hansenne M, Pitchot W, Ansseau M. Serotonin, personality and M. Hansenne, W. Pitchot,
borderline personality disorder. M. Ansseau
Acta N europsychiatrica 2002: 14:66–70. CBlackwell Munk sgaard University of Lie
`ge, Department of Psychiatry, Lie
`ge, Belgium
2002
Serotonin is one of the neurot ransmitters implicated in nor mal
per sona lity. M any psychobiological models of per sonality include
some dimensions related to seroton in. For inst ance, the ha r m
avoidance dimension of the biosocial model developed by Cloninger
is related t o sero tonergic activity. Higher scores on the har m
avoidance dimension should theoretically reflect increased
serotonergic activity. H owever, correlat ion stud ies related serotonin
activity to harm avoidance dimension have not yielded consistent
findings. T hese con troversial results are p robab ly related to t he
complexity of the neurotr ansmitter systems, and the different
assessment techniques used in these studies. Finally, recent genetic
studies have examined the association b etween personality
dimensions and serotonergic recept or polymor ph isms with mixed
results. Serotonin is not only related to some dimensions of normal
per sona lity. Several psychopat hological disorder s are associated
with serot oner gic dysfunct ion. M ore par t icularly, b orderline
per sona lity disord er (BPD ) can b e defined by ma ny of the
symptoms associated with serotonergic dysregulation, includ ing
affective lability, suicidal behaviour s, impulsivity and loss of
impulse cont rol. Indeed , several reports have demonstr a ted the
efficacy of selective serotonin re-uptake dru gs in t reating th e
depressive and impulsive sympt oms o f patients with BPD. M oreover, Keywords: serotonin; personality; borderline personality
some cha llenge studies have rep orted a lower seroto nergic act ivity disorder
in BPD. Because t hese cha llenges are n ot specific, we have assessed
Correspondence: Michel Hansenne PhD, University of Lie
`ge,
the seroton ergic activity in BP D with t he flesinoxa n challenge. Department of Psychiatry, CHU Sart Tilman (B35),
Preliminar y result s showed tha t the prolactine responses to flesinoxan B-4000 Lie
`ge, Belgium.
were significantly lower in BPD pat ients compared to t hose Tel: 00 32 4 3667960; Fax: 00 32 4 3667283;
observed in controls. E-mail: Michel.Hansenne/ulg.ac.be
Introduction
Serotonin is one of the neurotra nsmitt er s impli-
cated in no r m al personality. M a ny psychobiologi-
cal models of p er so nality includ e some dimensions
related to serotonin. For instance, in the Zucker-
man model of personality (1), the dimension of im-
pulsive unsocialized sensation seeking (ImpU SS) is
negatively cor related with serot oner gic d imension.
Again, the har m avoidance dimension of the bi-
osocial m odel d eveloped by Clo ninger (2) is related
66 cBlackwell Munksgaard, Acta Neu ropsy chiatr ica, 14 ,2,66–70
to serotonergic activity. Serotonin is not only re-
lat ed t o some dimensions of normal person ality.
Several psychopath ological disorder s a re associ-
ated wit h serot onergic dysfunction. More par t icu-
larly, borderline personality disorder (BPD ) can be
defined by ma ny of the symptoms associated with
serotonergic dysregulation, including affective la-
bility, suicidal behaviours, impulsivity and loss of
impulse control. This review presents some recent
findings on serot onin, personality and BPD. M ore
particularly, t his review focuses on the bioso cial
Serotonin, personality and BPD
model of Cloninger and o n the flesinoxan chal-
lenge t est.
Serotonin and personality
Cloninger and colleagu es have proposed a bioso-
cial model of personality based on fou r temp era-
ments (novelty seeking, harm avoidance, reward
dependence and persistence) and three characters
(self-directedness, cooperativeness and self-tran -
scendence) (3). N ovelty seeking is defined as the
tendency to respond actively to novel stimuli lead-
ing to pursuit of rewards an d escape from punish-
ment. Harm avoidance corresponds to the
tendency toward an inh ibitor y response to signa ls
of aversive stimuli that lead to avoidance of pun-
ishment a nd non-reward. Reward dependence is
defined as the ten dency fo r a positive response to
signals of reward to mainta in or resist behavioural
extinctio n. Persisten ce is described in ter ms of per-
severance despite frustrat ion a nd fat igue. Self-di-
rectedness refers to the ability of a n individua l to
control, regulate and adap t his behaviou r to fit the
situation in accord with individua lly chosen goals
and values. Coo pera tiveness is for mulated to ac-
count for individual differences in ident ification
with and acceptance of other people. Self-tra n-
scendence is a charact er istic associated with spiri-
tuality, and refers generally to identification with
everything conceived as essential and con sequen-
tial parts of a unified whole. The temperament and
character inventory (TCI) is a 226-item self-ques-
tionnaire developed by Cloninger an d colleagues
to assess the seven dimensions o f person ality (4).
According t o this model, three o f the four tem-
peraments were associated with a specific central
neurotransmitter. Novelty seeking was theoretic-
ally associated to dop aminergic activity; ha r m
avoidan ce to serot onergic activity; and reward de-
pendence to noradren ergic activity. More par t icu-
larly, higher scores on the har m avoidance
dimension should theoretically reflect increased
serotonergic activity. This is directly suppor t ed by
the fact that an inverse relationship was noted be-
tween aggression and har m avoidan ce, as well as
between aggression and central 5-HT functioning
(5,6).
The relationship between harm avoidance and
serotonergic activity has been evaluated in several
studies. Pfohl et a l. (7) have described a higher
score of th e har m avoidance dimension in obsess-
ive-compulsive disorder (OCD) patients compared
to controls, but without any association between
this dimension and plat elet imipramine b inding. I n
another study, the score of the harm avoidance di-
mension was higher in a group of bulimic wo men
67
compared to nor ma l wom en, but t he whole blo od
serotonin levels were no t related to this dimension
(8). In t he study by L imson et al. (9) there were no
significant co rrelations between cerebro spina l fluid
concent rations of t he serotonin metabolite 5-hy-
droxyind oleacetic acid and har m avoidance scores.
However, given the complexity o f the neurotra ns-
mitter systems, these studies cannot be considered
as evidence against a relationship between sero-
tonergic activity and t he har m avoidance dimen-
sion. In cont rast, N elson and Cloninger (10) have
demonstrated that harm avoidance and reward de-
pendence scores were found to significantly predict
the response t o the 5-HT2 recepto r anta gonist and
5-HT reup take inhibito r an tidep ressant nefazo-
done in depressed patients. More recently, Gerra
et al. (11) foun d tha t harm avoidance scores cor re-
lated significantly with prolactin (PR L) response
to d-fenfluramine in healthy volunteers.
Recently, our group has developed a serotonergic
challenge test using flesinoxan (12). Flesinoxan is a
highly pot ent and selective 5-HT1A agonist in-
ducing a significant and dose-dependent release of
PRL and cortisol in normal subjects. In contrast,
depressed pat ients exhibited a blunt ed cortisol re-
sponse, and m ore p articula rly those with a history
of suicide a ttempts. F lesinoxan challenge was a
goo d ca n d id a t e to a ssess the relationship between
har m avoidance a nd serot onergic activity. In a fir st
study (13), we have reported a positive association
between the PRL response to flesinoxan a nd the
harm avoidance dimension in a group of depressed
patients. This result appears consistent in light of
the studies noted above. However, a major pitfall of
this study was the state dependence of harm avoid-
ance dimension in depression. Indeed, as harm
avoidance has been shown in this and other studies
(14,15) to correlate with the severity of depression,
the positive relationship between harm avoidance
and t he PRL respo nse to flesinoxan could b e due to
th e depressive sta tus. Therefore, th e same design h as
been carried out in a sample of non -depressed sub-
jects (16). This second study o stensibly replicat es
and extends t he first one (13) an d is consistent with
the results of G erra et al. (11)
However, an important limitation of these
studies is the selective effect of flesinoxan o n th e
5-HT1A recept ors. Ind eed, the pharmacologically
induced PR L response to flesinoxan is an indirect
ind ex of serot onergic neurotra nsmission a nd could
involve area s of the br a in not related with t h e neu-
ral substrat e of har m avoida nce hypot hesized by
Cloninger. M o reover, the lack o f a placebo-con-
trolled flesinoxan challenge limits th e conclusions
of this stud y. Th erefore, to examine exha ustively
the hypothesized link between har m avoida nce and
Hansenne et al.
serotonergic activity, futu re studies should be con-
ducted using agonist and antagonist serotonergic
agents in non-pa tient gro ups.
The association b etween serotonergic function
and harm avoidance dimension of the Cloninger
model wa s also investigated using genetic markers.
Indeed, recent genetic st udies have examined th e
association between personality dimensions and
serotonergic recepto r polymorphisms with mixed
results. No association was observed between indi-
viduals grouped by th e long a nd sho r t for ms of
the serotonin transporter gene and the personality
dimension of har m avoidan ce (17). In contra st, an
association between harm avoidance and the short
for m of the serotonin t ransporter gene (5-
HTTLPR) has been reported in another study
(18). In a recent stu dy, no con tribution of the 5-
HTR2a polymorphism on harm avoidance per son-
ality trait emerged (19).
Serotonin and BPD
BPD is defined in DSM -IV (20) as ‘a patter n of
instab ility in interpersonal relationships, self-im-
age, and affects, and mar ked imp ulsivity’. The syn-
drome of BPD may be classified into four groups
of symptoms: affective, impulsive, ego/inter p er-
sonal an d psychotic. Several of t hese symptom s are
associat ed with seroto nergic dysfunction, and
more particularly a ffective lability, suicida l behav-
iours and impulsive aggression. Based on this
sta tement , serotonin upt ake inhibitors were
studied openly in BPD pa tient s soon aft er the re-
lease o f flu oxetine. Th ree reports have demon-
strated t he efficacy of fluoxetine in treating the
depressive and impu lsive sympt oms of patients
with BPD (21–23). However, these stu dies were not
double-blind, which could lead to bias in collecting
the dat a. The first d oub le-blind, placebo-con-
trolled study conducted among a small group of
BPD pat ients demonstrated clear efficacy for
fluoxetine over placebo alo ng a number of dimen -
sions, including d epression, anxiety and global
function (24). The second controlled fluoxetine
study among BPD pat ients repo r ted improvemen t
in a number of symptoms, but this improvement
was not st atistically significant, except fo r ag-
gression against objects (25). In another contro lled
tr ial in 40 out -patients with personality disorders
including 13 with BPD, fluoxetine had a n anti-ag-
gressive effect on impulsive aggressive individuals
with personality disorder including BPD (26). I n
an open tr ial with sertr aline, significant redu ction
in irr itability and aggression were repor ted in BPD
(27). Significant improvement of BPD patients was
68
also reported with venlafaxine (28). H owever, more
con tro lled trials with larger patient po pulatio ns
are necessary to replicate these results.
Platelet studies have been carr ied out in BPD to
assess the serotonergic function in this disorder.
Platelet 5-HT was higher in patients with BPD
than in non-bord erline patients and nor mal con-
trols, and was positively correlated with the dispo-
sition to exp erience anger (29,30).
Another way to assess fur ther the role of th e 5-
HT function in BPD is the use of specific phar ma-
cological probes. Cocar ro et al. (5) administered
the non -specific 5-HT releaser/reupta ke b locker
fenfluramine to p atients with major depressive dis-
order s and/o r personality disorders including BPD
and foun d that PR L respo nse was blunted com-
pared to non -borderline perso nality disorder an d
normal control subjects, independent of the co-
morbidity o f major affective disord er. M oreover,
PR L response was negatively cor related with im-
pulsive aggression and with histor y of suicide
attempts. In contrast , M a r tial et al. [31] have re-
ported higher PRL response and lower cor tisol re-
sponse to fenflura mine in five BPD women
compa red to cont rols. Recently, Soloff et al. (32)
performed a st udy using positron-emission tomo-
grap hy (PET) during a fen flura mine challenge test
in BPD. Th e results shown tha t patients with BPD
have lower responses to serotonergic stimulation in
areas of prefrontal cortex, a region a ssociat ed with
regulation o f impulsive behaviour. Hollander et al.
(33) found higher cortisol levels and mar ginally
blunted PR L response to the partial 5-HT agonist
meta-chlorophenylpipera zine (m-CPP) in eight
male pat ients with BPD comp ared to contro ls.
However, the result s amon g women (four subjects)
are no t significant. This gender difference, as no ted
by the a uthors, might b e attr ibut able t o circulat ing
ovarian hormones. The authors also reported that
m-CPP ind uced a distinctive spacy (deper sona l-
ized/deua lized) and high (euph oric) behavioural
reaction in the p atients. The same group found in
a larger samp le of BPD patients a significant as-
sociation between th e presence of a spacy and high
behavioural response to m-CP P and increased
PR L and cortisol peak on m-CPP challenge (34).
In anot her study with m-CPP, women with a BPD
diagnosis had PRL and cor tisol blunted responses
to this cha llenge (35). Fu r thermo re, these aut hors
repor ted a significan t negat ive correlation between
delta peak PRL values and abuse characteristics,
such as the severity and duration of physical and
sexual abuse. They conclud ed tha t the a ltera tion
of t he serotonergic system was probably no t re-
lated to t he BPD diagnosis per se,buttosustained
traumatization during childhood.
Serotonin, personality and BPD
Since these cha llenges are not specific, we have
assessed the serotonergic activity in BPD with the
flesinoxan ch allenge test. Th is preliminary stud y
was con ducted among 20 BPD pat ients (14
women) with a mean age of 30.5 years (SD Ω10.2)
and 20 healthy volun teers matched for gender with
a m ean age o f 37. 9 year s (SD Ω9.6). The age differ-
ence between the two group s was significant (ZΩ
ª2.27, PΩ0.02). T he diagnosis of BPD was
based on the D SM -IV criteria and on the self-
questionnaire from t he Str uctured C linical Inter-
view for DSM -III Axis II (SCID -II ). According
the D SM -IV cr iteria, 16 BPD patients had a cur-
rent diagno sis of major depressive disorder, and
four had a n eating disorder. The patients were free
of medication at least 2 weeks before th e challenge.
Because of th e influence of oestrogen on the pro -
lactin levels during t he men strual cycle, th e flesi-
noxa n challenge test was perfo r med between the
third a nd the 12th day of the menstrual cycle. The
Ethical Committee of the University of Lie
`ge
Medical School approved the protocol and all sub-
jects gave their informed consent. There was a sig-
nifica nt d ifference bet ween BP D p at ients (40627 ∫
21042 mIU min/mL) and healthy volunteers
(75546 ∫46612 mIU min/mL) for PRL respon se to
flesinoxan (ZΩª2.92, PΩ0.003). Among the
BPD patients, PR L response to flesinoxa n was
lower in patients with pa st history of suicide
attempts (NΩ8) comp ared to patients with a nega-
tive history (P٪3.04, P!0.002). Because flesi-
noxa n stimulates specifically the 5-H T1A
postsynaptic receptors, these results suggest tha t
BPD patients are character ized by lower 5-HT 1A
recept or sensitivity. Overall, th is stud y is consistent
with previous studies that have reported lower
PRL response to serotonergic challenge tests.
Some limita tions o f the study should be ack nowl-
edged. F irst, the lack of a placebo-contro lled fles-
inoxan challenge limits the conclusions of this
stu dy. Anot her imp ortant limitatio n of this stud y
is the use of a self-repor t questionnaire t o assess
Axis II d iagnoses. G iven the complexity of person-
ality pat hology, a structu red interview schedule
would have been preferable. Th e comorbidity be-
tween Axis II and Axis I diagn ostic limits also the
con clusions. T he PR L blunted resp onse obser ved
among BPD pa tient s could be due t o the co -
morbidity o n Axis I, a nd more particular ly with
major depressive disorder. However, some studies
have reported t hat PR L response to flesinoxan did
not differ between depressed pa tient s and con trols,
but that PRL response was lower in a subgroup
of depressed patients characterized by past suicidal
history (36). A final limitat ion is the lack of beha -
vioural assessment fo r impulsivity, irritability.
69
Conclusions
Ta ke n t o get h er , t h e d a t a r ep o r t ed a bo ve su p p o r t t h e
implication of serotonin in b oth nor ma l an d dis-
ordered personality. More specifically, serotonergic
activity is related with t he har m avoida nce dimen-
sion of the model developed by Clonin ger. H owever,
some resu lts are not consist ent with t his relation-
ship. T his may indica te that the relatio n bet ween
serotonin and ha r m avoidance is indirect, with the
contribution of other neurot ransmitt er systems. An
alter native hypo thesis is the heterogeneity of the
subjects included in these studies an d the different
tolls for serotonin assessment. Co ncerning BPD, t he
results reported here show a major implication of
th e serotonergic function in the aet iology of th is dis-
order and are consistent with previou s studies which
linked lower seroto nergic activity and impulsivity.
These findings provide interesting track fo r the
pharmacological treatment of this dramatic dis-
order. However, more controlled studies with larger
patients populations are necessary to replicate the
results of existing research.
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