Cognitive and emotional characteristics of alexithymia
A review of neurobiological studies
Junilla K. Larsen
*, Nico Brand
, Bob Bermond
, Ron Hijman
Department of Health Psychology, Utrecht University, Postbus 80140, Utrecht 3508 TC, Netherlands
Department of Neuropsychology, University of Amsterdam, Amsterdam, Netherlands
Department of Psychiatry, University Medical Center of Utrecht, Utrecht, Netherlands
Received 7 November 2001; accepted 29 April 2002
Objective: To review neurobiological studies of alexithy-
mia in order to achieve a better understanding of the relation-
ship between alexithymia and psychosomatic diseases and
psychiatric illnesses. Methods: Neurobiological studies of
alexithymia were reviewed with a special focus on how emo-
tional and cognitive elements of alexithymia are reflected in
earlier research. Results: Studies that have correlated alexithy-
mia to corpus callosum dysfunctioning have mainly found
impairments in cognitive characteristics of alexithymia, whereas
from studies of right hemisphere and frontal lobe deficits, it
may be concluded that both cognitive and emotional character-
istics of alexithymia are impaired. Conclusion: The fact that
there is no general agreement on how to define alexithymia
seems to have hampered theoretical and empirical progress on
the neurobiology of alexithymia and related psychosomatic
diseases and psychiatric illnesses. Alexithymia should no longer
be approached as one distinct categorical phenomenon and
follow-up studies should monitor subjects according to both
the cognitive and emotional characteristics of alexithymia.
D2003 Elsevier Inc. All rights reserved.
Keywords: Alexithymia; Neurobiology; Right hemisphere; Commissurotomy; Interhemispheric transfer; Frontal lobe
Definition of alexithymia
Over the past two decades, there has been an expanding
scientific interest in the regulation of emotion and in the
impact of dysregulated emotion on mental and physical
health . Alexithymia refers to difficulties in emotional
self-regulation and is thought to be one of several possible
risk factors in a variety of medical [2 – 7] and psychiatric
disorders [8– 17]. The alexithymia concept stems from the
field of the psychology of emotions and psychosomatics. A
large proportion of patients with psychosomatic complaints
showed difficulties in emotional self-regulation. Sifneos
 introduced the term ‘alexithymia’ for these emotional
difficulties, which was derived from ‘‘the Greek alexis
(no words), thymos (emotion).’’ Five salient characteristics
of alexithymia have been described: (1) a reduction or
incapacity to experience emotions; (2) a reduction or inca-
pacity to verbalize emotions; (3) a reduction or incapacity to
fantasize; (4) an absence of tendencies to think about one’s
emotions; and (5) difficulty in identifying emotions [15,19].
From the first introduction of the term alexithymia, it
has been evaluated, criticized and refined. Whereas some
researchers regard the cognitive, evaluative aspects of
alexithymia as most important , others suggest that the
fundamental deficit in alexithymia is a limited — and in
extreme cases nonexistent — ability to consciously experi-
ence emotion . Drawing on recent knowledge from
neurobiology, Bermond [21,22] distinguishes two main
forms of alexithymia (Types I and II). Type I alexithymia
is characterized by the absence of the emotional experience
and, consequently, by the absence of the cognition accom-
panying the emotion. Type II alexithymia is characterized
by a selective deficit of emotional cognition with sparing of
emotional experience. Given the important psychological
differences between the two types of alexithymia, it is
suggested here that the classification into two types of
0022-3999/03/$ – see front matter D2003 Elsevier Inc. All rights reserved.
* Corresponding author. Tel.: +31-302-533027.
E-mail address: email@example.com (J.K. Larsen).
Journal of Psychosomatic Research 54 (2003) 533 – 541
alexithymia is useful towards examining the existing literat-
ure on the neurobiology of alexithymia, since it may offer an
explanation for the distinct neurobiological and related
physiological findings in the literature.
Measurement of alexithymia
Many of the early studies on alexithymia are of ques-
tionable validity, as they were conducted with measures that
were shown to lack reliability and validity, such as the
Schalling Sifneos Personality Scale (SSPS) and the MMPI
alexithymia scale . For several years, however, the
Toronto Alexithymia Scale (TAS) has proven to be the most
reliable and valid method for measuring several character-
istics of alexithymia [23 – 25]. The TAS demonstrated a
replicable four-factor structure: difficulty identifying feel-
ings (Factor 1); difficulty describing feelings (Factor 2);
reduced daydreaming (Factor 3); and a tendency to think in
externally oriented ways (Factor 4). Since the items assess-
ing daydreaming showed little coherence with the other
factors, two successive revisions of the scale have led to the
20-item Toronto Alexithymia Scale (TAS-20), eliminating
all items assessing imaginal activity [26 – 28].
Recently, the validity and reliability of a new instrument
to assess alexithymia, the Bermond– Vorst Alexithymia
Questionnaire (BVAQ), have been established [29,30].
The BVAQ contains five subscales: (1) emotionalizing, (2)
fantasizing, (3) identifying, (4) analyzing and (5) verbaliz-
ing emotions. Analogous to the distinction in cognitive and
emotional aspects of alexithymia within the hypothesized
subtypes of alexithymia [21,22], the subscales of the BVAQ
exhibit a second-order (two-factor) structure, with the sub-
scales emotionalizing and fantasizing representing an emo-
tional component, and the subscales identifying, analyzing
and verbalizing emotions representing a cognitive compon-
ent of alexithymia, respectively. The total TAS-20 score
shows high correlations with the cognitive, but not the
emotional, component of the BVAQ [29,30]. Both difficulty
fantasizing and difficulty emotionalizing within the BVAQ
remained statistically uncorrelated with the total TAS-20
and weakly correlated or uncorrelated with the TAS-20
subscales . Therefore, as a diagnostic instrument, the
TAS-20 may emphasize the cognitive and underestimate the
emotional component of alexithymia. It is suggested here
that both the original and revised versions of the TAS
emphasize the cognitive component of alexithymia, since
most, if not all, factors of the TAS represent cognitive
characteristics of alexithymia.
Alexithymia has often been attributed to neurobiological
dysfunctioning. Some studies found evidence for dysfunc-
tioning of the corpus callosum in alexithymia, whereas
other studies found a relationship between alexithymic
characteristics and dysfunctioning of the right cerebral
hemisphere, anterior cingulate cortex (ACC) or the orbito-
frontal cortex. The aim of this article is to review neuro-
biological studies of alexithymia in order to achieve a
better understanding of the relationship between alexithy-
mia and psychosomatic diseases and psychiatric illnesses.
To that aim, neurobiological studies of alexithymia were
reviewed with a special focus on how emotional and
cognitive elements of alexithymia are reflected in earlier
research, seeking evidence for the two main forms of
alexithymia as originally defined by Bermond .
Alexithymia and neurobiological dysfunctioning
Several models have been proposed to explain how the
brain mediates emotion. A parsimonious and convincing
model states that the right hemisphere is more involved than
the left in all aspects of emotional behavior [31,32]. This
model is largely based on the fact that in most people, the
verbal, conscious and serial information processing takes
place in the left hemisphere [33,34], while the unconscious,
nonverbal and emotional information processing mainly
takes place in the right hemisphere [35 – 38]. From this
model, two neurobiological views on alexithymia have been
derived: (A) alexithymia is the result of a deficit in inter-
hemispheric communication, involving the corpus callosum
[39– 42]; and (B) alexithymia is the result of a dysfunction
of the right cerebral hemisphere [43,44]. Another model
states that the brain organizes emotion differently as a
function of valence, with positive emotions mediated by
the left hemisphere and negative emotions by the right
hemisphere . This model has been further expanded
by Davidson et al. , who postulate that the existence of
separate approach (correlating with positive emotion) and
withdrawal systems (correlating with negative emotion) is
lateralized to the left and right frontal lobes, respectively
. A third neurobiological hypothesis has been derived
from this model: (C) alexithymia is the result of dysfunc-
tional mechanisms in the frontal cortex. The above-men-
tioned models should be considered more as attempts at
systematization, aiming to classify neurobiological studies
on alexithymia, than as firmly established theories.
Corpus callosum dysfunctioning
According to Gazzaniga and LeDoux , cognitive
components of stimuli presented to the right hemisphere
reach the conscious left hemisphere directly by means of the
corpus callosum, while the emotional value is first projected
downward to the limbic system and from there reaches the
left hemisphere by the anterior commissure. Consequently,
blockage of the function of the corpus callosum can result
into a specific type of alexithymia (Type II), in which a
person still experiences basic emotional feelings, but has no
conscious cognition concerning these feelings . The
hypothesized relationship between blockage of corpus cal-
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541534
losum functioning and Type II alexithymia has been strength-
ened through the descriptions of persons with corpus cal-
losum transsections [47,48]. When emotional stimuli were
presented to the right hemisphere of these persons, they were
unable to verbalize their emotional feelings, whereas from
nonverbal reactions, it was clear that emotional feelings had
been induced. On the basis of the reasoning of Gazzaniga and
LeDoux, it should be expected that in case of complete
cerebral commissurotomy, i.e., sectioning both the corpus
callosum and the anterior commissure, there should be
deficits in both emotional and cognitive aspects of alexithy-
mia. In a preliminary investigation of 12 split-brain individ-
uals, Hoppe and Bogen  observed that patients following
complete cerebral commissurotomy for intractable epilepsy
developed a decreased capacity for fantasy, a pronounced
operative style of thinking and difficulties in describing
feelings. While the pronounced operative style of thinking
and difficulties in describing feelings are cognitive character-
istics of alexithymia, the decreased capacity for fantasy is an
emotional aspect of alexithymia . Thus, these results are
in line with the hypothesis that complete cerebral commis-
surotomy would lead to deficits in both cognitive and
emotional aspects of alexithymia.
TenHouten et al. [40,49,50] compared the spoken and
written responses of eight patients who underwent cerebral
commissurotomies with those of eight neurologically intact
control subjects to a film that was aimed at evoking
emotions. In comparison with the control subjects, commis-
surotomized patients showed a decreased capacity for fant-
asy and use of symbols (emotional aspects of alexithymia)
and difficulties in describing feelings (cognitive aspect
As a result of the studies with split-brain patients,
researchers have become interested in the relationship
between alexithymia and interhemispheric transfer (corpus
callosum functioning). Studies have been performed in
which alexithymic and nonalexithymic patients have been
compared on interhemispheric transfer through the corpus
callosum. Support for the interhemispheric communication
deficit hypothesis of the cognitive component of alexithy-
mia was provided by studies using a tactile finger local-
ization task to assess the efficiency of interhemispheric
communication [42,51]. This task requires the transfer of
information across the corpus callosum for successful per-
formance, since fine sensorimotor information from the
fingers is conveyed to the contralateral hemisphere. It has
been shown that split-brain patients perform poorly on this
A study by Zeitlin et al.  compared the efficiency of
interhemispheric transfer in 15 alexithymic and 7 nonalex-
ithymic patients suffering from posttraumatic stress disorder
(PTSD) and 10 controls in using the tactile finger local-
ization task. Alexithymia was assessed by the total TAS
score, emphasizing the cognitive aspects of alexithymia. A
strong association was found between the TAS global
alexithymia score and the lack of bidirectional interhemi-
spheric transfer. Parker et al.  also found a strong
association between the TAS global alexithymia score and
a bidirectional deficit in interhemispheric transfer. From
both studies, it appeared that the deficit in interhemispheric
communication in the cognitive alexithymic patients was
not as great as in commissurotomy patients. A possible
explanation for this is that the tactile finger localization task
is not the most appropriate way to assess a deficit in
interhemispheric communication associated with emotional
processing . Another explanation is that in the non-
commissurotomized alexithymic patients, the disconnection
is less absolute and more functional in nature. In an
extension of the study of Zeitlin et al. , Dewaraja and
Sasaki  examined the relationship between interhemi-
spheric transfer and alexithymia using both linguistic and
nonlinguistic Japanese symbolic stimuli. Alexithymia was
assessed using the MMPI alexithymia scale and the Schal-
ling Sifneos Personality Scale — Revised (SSPS-R). While
both instruments have proven unsatisfactory psychometric
qualities , their factors point mainly to a cognitive
deficit in alexithymia (i.e., capacity to describe feelings,
preference for describing events in detail and the ability to
communicate with others). Whereas Zeitlin et al.  found
a bidirectional relationship between cognitive aspects of
alexithymia and the callosal transfer process, Dewaraja and
Sasaki  found a unidirectional (right-to-left) relation-
ship. The processing of linguistic information is known to
be mainly associated with the left hemisphere, while sen-
sorimotor processing is not known to be associated with a
particular hemisphere. Therefore, the finding of a unidir-
ectional relationship by Dewaraja and Sasaki  may be
more significant regarding the concept of alexithymia.
In a recent study, the relationship between the cognitive
Type II alexithymia and interhemispheric transfer deficit
was examined  using the BVAQ. The EEG was con-
tinuously recorded from homologous occipital, parietal,
temporal and frontal recording sites during the presentation
of films excerpts, one of neutral and two of emotional
content. An association was found between the cognitive,
but not the emotional, component of alexithymia and
Type II alexithymics, as compared to nonalexithymics,
had reduced coherence between the right frontal lobe and
the left hemisphere, independent of film. This result is also
in line with the reduction in interhemispheric alpha band
coherence found by TenHouten et al. [56,57] for commis-
surotomized patients. Because the corpus callosum appears
to be necessary for the transfer of more complex information
between the hemispheres, there is some indication for
reduced callosal function between the right frontal region
and the left hemisphere in Type II alexithymic individuals.
Dysfunctioning of the right cerebral hemisphere
In normals, right hemisphere advantage has frequently
been observed in the perception of emotion. Similarly,
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541 535
deficits in the perception of emotion have been found more
frequently in patients with right than left hemisphere
damage [58– 62]. Several studies have shown that individ-
uals with high levels of alexithymia are poorer than those
with low levels of alexithymia in the recognition of facial
expressions of emotions [20,43,44,63]. Since the ability to
recognize facial expressions of emotions is predominantly
linked to the right cerebral hemisphere, dysfunctioning of
the right cerebral hemisphere was suggested in alexithymia
[43,44]. Ross  and Fricchione and Howanitz  have
described studies of patients with large right unilateral
cortical lesions. These patients showed the symptoms of
a major depression, but denied feelings of depression.
After treatment with antidepressants, all expressive symp-
toms of a major depression disappeared, however, with the
exception of the mental emotional numbness. Thus, right
cortical lesions may result into the absence of affect,
representing the emotional component of alexithymia.
Following Bermond [21,22], the absence of the emotional
experience — and, consequently, absence of the cognition
accompanying the emotion — has been defined as Type I
alexithymia. Thus, right cortical lesions may result into
Type I alexithymia.
Although studies have been performed in which alex-
ithymic and nonalexithymic patients have been deliberately
compared on interhemispheric transfer, as far as we know,
no valid studies have been performed in which alexithymic
and nonalexithymic individuals have been directly com-
pared on functioning of the right cerebral hemisphere.
Conjugated lateral eye movements (CLEMs) have some-
times been used as an index of hemispheric activation, since
a predominance of eye movements in one direction is
thought to reflect activation of the contralateral hemisphere.
In a study of Parker et al. , the relationship between
CLEMs and alexithymic characteristics, measured by the
TAS, was examined. A positive relationship was found
between left hemisphere activation, indicated by a predom-
inance of right CLEMs, and the cognitive component of
alexithymia, as measured by a high global score on the TAS.
While the direction of CLEMs may be a function of an
individual’s consistent tendency to rely on a particular
cerebral hemisphere, there is evidence that the direction
can be influenced by the experimental situation and by the
type of questions asked. Moreover, much more research is
required to determine whether a possible tendency to rely on
the left hemisphere indeed represents a dysfunction of the
right hemisphere .
Frontal lobe dysfunctioning
Many studies have attributed the expressive components
of emotional processing to frontal lobe structures of the
brain. In a model that has been proposed to explain how the
brain mediates emotion, an interaction between emotional
valence and frontal lateralization has been suggested .
However, experimental studies of right-brain-damaged and
left-brain-damaged patients show that when the intrahemi-
spheric site of lesion was examined, anterior regions (i.e.,
frontal lobe) were more critical for emotional expression
than posterior regions, independent of valence . Stuss
et al.  describe many studies finding a decrease in
emotional expression after frontal lobe damage. Since a
reduction in emotional expression has also been described
for alexithymic patients , characteristics of alexithymia
may be the result of deficits in frontal lobe functioning.
However, the question remains as to which parts of the
frontal lobe will be specifically involved in cognitive and/or
emotional characteristics of alexithymia.
Higher cognitive and affective functions are mainly
localized in the prefrontal cortex, which occupies approx-
imately 30% of the total amount of cortical space. The
prefrontal cortex can grossly be divided into dorsolateral
and ventromedial regions. The ventromedial frontal area
(Brodmann’s areas 24, 25, 32, 11, 13 and 14) is connected
with limbic structures in the medial temporal lobe, and
hence is well situated to integrate motivational and emo-
tional processes. Both the orbitofrontal cortex and the
ACC are located in the ventromedial frontal area and
are especially important for emotional functioning [70,71].
Analysis of the orbitofrontal cortex and ACC suggest that
these regions are involved in emotion-related learning
. In modern approaches to emotion, emotions are
often considered to be states elicited by rewarding and
punishing stimuli, so that any failure to alter behavior
when the reinforcement value of environmental stimuli
changes will lead to impairments in inappropriate emo-
tional experience and related behavior . Electrical
stimulation of the orbitofrontal cortex produces many
autonomic responses  and, moreover, orbitofrontal
lesions are associated either with a blunting of emotional
responses, including the attenuation of autonomic accom-
paniments of emotion, or intense expression of affect with
loss of inhibitions . Emotionally disturbed alexithymic
individuals resemble the blunted rather than the disinhi-
bited type. Lesions of the ACC have also been associated
with emotional aspects of alexithymia, such as blunting of
emotional experiences [75,76]. In addition, it was found
that the reduction in emotional experience in a group of
patients with ventral frontal lobe damage was correlated
with impairments in the identification of facial and vocal
emotional expression , merely reflecting cognitive
characteristics of alexithymia.
Since normal subjects’ emotional awareness was asso-
ciated with greater activation in the ACC during elicitation
of film- and recall-induced emotion , it was hypothe-
sized that deficits in ACC activity are associated with
alexithymia. This hypothesis was tested in a comparative
study of the cerebral regions activated during viewing of
emotional stimuli in a group of high and low alexithymic
males . Intergroup comparisons revealed that alexithy-
mics had higher activation associated with positive pic-
tures, but showed no effect of arousal with negative
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541536
pictures. Main differences were concerned with medial
prefrontal (Brodmann’s area 9) and ACC regions. Al-
though these findings should be considered preliminary
until they are replicated, they might suggest that positive
and negative emotions should be treated in a different
manner in Type I alexithymic patients. Hornak et al. 
studied 10 patients with ventral prefrontal lesions and
observed that all reported changes in their ability to feel
emotions compared to their premorbid state. However,
the extent to which there were changes (increases or de-
creases) in the capacity to feel negative or positive
emotions was quite variable across patients. It is possible
that different subregions within the ventromedial prefron-
tal cortex could be associated with the elaboration of
different types and intensity of emotion, consistent with
its role in integrating information about rewards and
punishments. In conclusion, there appear to be distinct
regions in the ventromedial prefrontal cortex, such as the
ACC and the orbitofrontal cortex, that participate in
emotion and that may be associated with impairments in
both cognitive and emotional aspects of alexithymia,
reflecting Type I alexithymia.
Local depletion of dopamine in parts of the prefrontal
cortex by application of 6-OHDA produces effects on
emotions similar to those of lesions [70,79]. Dopamine
neurons are mainly organized in the substantia nigra, which
contains over 90% of the dopamine cells and mainly
projects to the striatum. It is now generally accepted that
the basal ganglia, in addition to movement control, fulfill
important functions in emotions . Two basal ganglia
neural circuits have been described: the dorsolateral pre-
frontal circuit and the lateral orbitofrontal circuit (for
detailed descriptions, see Ref. ). The basal ganglia are,
therefore, well connected with prefrontal structures that
fulfill important functions for the emotional experience.
Furthermore, it may be assumed that these circuits are
modulated by dopamine, since the substantia nigra partic-
ipates in both circuits . In line with this, Parkinson
patients, in whom the functions of nigrostriatal dopamine
circuits have been reduced, show numbness in affect and
motivation. This numbness in affect and motivation is
related to the reduced dopaminergic activity in the prefrontal
cortex . Overall, depletion of dopamine in the ACC or
the orbitofrontal cortex may produce both cognitive and
emotional characteristics of alexithymia, defined by Ber-
mond [21,22] as Type I alexithymia.
Alexithymia, sympathetic activity, somatic diseases and
Based on preliminary findings in the mid-1980s, it was
suggested that alexithymia is related to illness because it
produces hyperarousal to situational stressors [82,83].
Whereas in some studies alexithymia was associated with
higher tonic or baseline levels of sympathetic activity [84 –
86], other studies found either hypoarousal or normal
arousal during exposure to a stressor [87 – 89]. A possible
explanation for these different results may be that different
types of alexithymia formed by distinct neural malfunction
produce different levels of sympathetic activity.
Lesions of the corpus callosum may result into higher
sympathetic activity, since patients with corpus callosum
deficits can be affected by several situations without having
any explanation for their feelings . Therefore, they will
experience prolonged stress and related physiological hyper-
arousal, which may be a risk factor for a variety of
psychosomatic diseases and psychiatric illnesses. No studies
on the physiology of corpus callosum deficits have been
performed so far. However, data from brain-damaged and
normal subjects strongly suggest that the right hemisphere is
more closely related to the autonomic nervous system, and
thus, more intimately linked with the physiological and
automatic components of the emotions than the left hemi-
sphere [90,91]. Heilman and Gilmore  have suggested
that the right hemisphere is more in touch with subcortical
systems that are important for arousal and intention. More-
over, it appears that cerebral arousal is mediated by nor-
epinephrine (NE), which, although widespread, is mainly
supposed to be innervated by right hemispheric pathways
. On the basis of these findings, it may be expected that
alexithymia produced by right hemisphere deficits is asso-
ciated with reduced physiological responses. With respect to
the orbitofrontal cortex, it has been demonstrated that
electrostimulation of this area results in a great number of
autonomic and endocrine responses  and that lesions of
this area result in reduced physiological responses
[70,94,95]. It is, therefore, suggested that alexithymia due
to orbitofrontal lesions or a reduced neural or dopaminergic
innervation of this area also results in reduced emotional
physiological responses .
Overall, it can be stated that it is impossible to predict the
level of the emotional physiological responses without
knowledge on which neural malfunction alexithymia is
based, since facilitation as well as inhibition may be
expected. This is clearly illustrated in a study of Henry
et al.  demonstrating that, although the mean level of
sympathetic activation (as measured by 3-methoxy-4-
hydroxyphenylethylene glycol levels, MHPG) in alexithy-
mic patients is in the normal range, the MHPG levels of
16 of 17 patients studied were either clearly above or below
that normal range.
(Psycho)somatic diseases and psychiatric illnesses
Neafsey  refers to literature demonstrating that the
risk for psychosomatic diseases is reduced after prefrontal
lesions. Moreover, it is suggested here that the reduced
physiological responses due to deficits in the right hemi-
sphere will also result into a reduction of psychosomatic
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541 537
diseases. Therefore, alexithymia due to impairments in both
the right hemisphere and the prefrontal cortex (Type I) may
be associated with a reduction in psychosomatic diseases.
However, it is assumed that alexithymia produced by corpus
callosum dysfunctioning (Type II) is associated with a
variety of (psycho)somatic diseases. This association may
be the result of a misinterpretation of the somatic sensations
that accompany emotional arousal. It is also possible that the
association between alexithymia and somatic diseases is due
to sustained arousal and chronic dysregulation of the
physiological component of emotion response systems. As
a result of stimulation of the sympathetic nervous system
(SNS), elevated levels of adrenaline and noradrenaline may
influence the immune system indirectly via a-andb-
adrenergic receptors that have been found on immune cells
and organs . In agreement with this, some research has
found an association between alexithymia and reduced
levels of immunity [98,99]. Dewaraja et al.  found that
highly alexithymic men had a significantly lower number of
cells of the cytotoxic natural killer (NK) subset. These
results suggest that the negative modulation of cellular
immunity, combined with other factors, results in the
association between alexithymia and somatic diseases.
Alexithymia has been associated with a variety of
(psycho)somatic diseases, including functional gastrointes-
tinal disorders and chronic pain [2 – 7]. Moreover, several
researchers have explored the relationships between alex-
ithymia and psychiatric illnesses. Empirical studies have
reported elevated levels of alexithymia in individuals with
eating disorders, such as anorexia nervosa and bulimia
nervosa [8– 11]. Moreover, several studies have found a
strong positive correlation between alexithymia and depres-
sion in normal [12,13] as well as clinical samples [14,15]
and, furthermore, empirical studies have found elevated
levels of alexithymia in patients with panic disorders
[16,17] and PTSD . Although many studies found
varying correlations between alexithymia and psychiatric
different characteristics of alexithymia could be differenti-
ated. With reference to possible psychiatric complaints,
such a differentiation is important. Although Type I alex-
ithymics do experience a host of problems, they are — due
to the seriously reduced level of emotionalizing — still free
from emotional problems , whereas Type II alexithy-
mics do mention such problems. This is understandable
since they do get emotionally aroused, but cannot — due
to the lack of emotion accompanying cognitions — under-
stand the felt emotional arousal, resulting in further emo-
tional problems . Moreover, because of the cross-sectional
design of most of the studies, it is not possible to make
any causal connection between alexithymia and the vari-
ous psychiatric illnesses. Prospective studies are needed
for that. From longitudinal studies, it appears that alex-
ithymia is a stable trait, in contrast to functional somatic
symptoms and psychological distress that change over
The focus of this study has been on current insights
into the different biological mechanisms of alexithymia.
Findings from research exploring the neurobiology of
alexithymia suggest that different features of alexithymia
are associated with a variation in brain organization.
However, the fact that there is no general agreement on
how to define alexithymia seems to have hampered
theoretical and empirical progress, as it has been a source
of confusion and misunderstanding. Some neurobiological
studies on alexithymia and emotion emphasize cognitive
aspects, and other studies emotional aspects, producing
different outcomes. In this article, neurobiological studies
on alexithymia were reviewed with a special focus on
how emotional and cognitive elements of alexithymia are
reflected in earlier research, seeking evidence for the two
main forms of alexithymia as defined by Bermond
From studies of split-brain patients, it can be concluded
that complete cerebral commissurotomy, i.e., sectioning
the corpus callosum and the anterior commissure, results
into distinct deficits in both cognitive and emotional
aspects of alexithymia. Studies in which neurological
intact subjects have been compared on interhemispheric
transfer through the corpus callosum [41,42,51,54] show
that specifically cognitive aspects, but not emotional
aspects, of alexithymia are associated with deficits in
interhemispheric transfer. Thereby, the findings of a uni-
directional relationship in the callosal transfer process
[41,54] may be more significant regarding the cognitive
characteristics of alexithymia. Following Bermond, it may
be concluded that Type II alexithymia, in which the
cognitive but not the affective component of alexithymia
is disturbed, is associated with a right-to-left unidirectional
deficit in interhemispheric transfer.
Studies of patients with right unilateral cortical lesions
show that these lesions often result into deficits in the
perception of emotion [58 – 62], which may be comparable
to deficits in cognitive characteristics of alexithymia. More-
over, right unilateral cortical lesions often result into emo-
tional numbness and mental emotional indifference
[32,64,65], which may be interpreted as impairments in
affective aspects of alexithymia. Thus, right unilateral
cortical lesions may be associated with Type I alexithymia,
characterized by the absence of the emotional experience
and, consequently, by the absence of the cognitions accom-
panying the emotion.
Many studies of patients with frontal lobe damage find a
reduction in emotional expression , which has also been
found in alexithymic patients . More specifically,
patients with orbitofrontal cortex and ACC lesions show
impairments in affective [70,73 – 76] and cognitive [73,78]
aspects of alexithymia. Thus, orbitofrontal cortex and ACC
lesions may result into Type I alexithymia, as originally
defined by Bermond [21,22], characterized (in its extreme
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541538
form) by the absence of the emotional experience and,
consequently, by the absence of the cognition accompany-
ing emotion. Since depletion of dopamine produces effects
on emotions similar to lesions, it is assumed that depletion
of dopamine in the lateral orbitofrontal circuit may also
result into Type I alexithymia. Since little direct research has
been done on the relationship among the right hemisphere,
the ACC, the orbitofrontal cortex and alexithymia so far, the
suggested link between these brain areas and Type I
alexithymia is rather premature.
We believe that the most important implication of the
reformulation of the alexithymia construct is that it provides
a better explanation for the physiological basis of the
association between alexithymia and physical disease. With-
out knowledge on which neural malfunction a specific type
of alexithymia is based, it is impossible to predict anything
meaningful about the level of emotional physiological
responses. So far, the research on the neurobiology of
alexithymia has mainly relied on indirect methods for
studying brain functioning. Additional research should
focus on the use of modern brain imaging techniques,
including magnetic resonance spectroscopy (MRS), positron
emission tomography (PET) and single photon emission
computed tomography (SPECT) to compare changes in
regional brain chemistry and brain activity between the
different types of alexithymic individuals and nonalexithy-
mic individuals during the elicitation and processing of
emotional states. Finally, alexithymia should no longer be
approached as one distinct homogenous phenomenon and,
subsequently, follow-up studies should measure the various
components of the alexithymia concept separately.
 Taylor GJ, Bagby RM, Parker JDA. Disorders of affect regulation:
alexithymia in medical and psychiatric illness. Cambridge: Cam-
bridge Univ. Press, 1997.
 Kauhanen J, Kaplan GA, Cohen RD, Salonen R, Salonen JT.
Alexithymia may influence the diagnosis of coronary heart dis-
ease. Psychosom Med 1994;56:237 – 44.
 Kauhanen J, Kaplan GA, Cohen RD, Julkunen J, Salonen JT.
J Psychosom Res 1996;41:541 – 9.
 Gage BC, Egan KJ. The effect of alexithymia on morbidity in hyper-
tensives. Psychother Psychosom 1984;41:136 – 44.
 Deary I, Scott S, Wilson JA. Neuroticism, alexithymia and medically
unexplained symptoms. Pers Individ Differ 1997;22:551 – 64.
 Lumley MA, Asselin LA, Norman S. Alexithymia in chronic pain
patients. Comp Psychiatry 1997;38:160 – 5.
 Porcelli P, Taylor GJ, Bagby RM, De Came M. Alexithymia and
functional gastrointestinal disorders: a comparison with inflamma-
tory bowel disease. Psychother Psychosom 1999;68:263 – 9.
 Bourke MP, Taylor GJ, Parker JDA, Bagby RM. Alexithymia in
women with anorexia nervosa: a preliminary investigation. Br J
Psychiatry 1992;161:240 – 3.
 Jimerson DC, Wolfe BE, Franko DL, Covino NA, Sifneos PE. Alex-
ithymia ratings in bulimia nervosa: clinical correlates. Psychosom
Med 1994;56:90 – 3.
 Schmidt U, Jiwany A, Treasure J. A controlled study of alexithymia
in eating disorders. Comp Psychiatry 1993;34:54 – 8.
 Cochrane CE, Brewerton TD, Wislon DB, Hodges EL. Alexithymia
in eating disorders. Int J Eat Disord 1993;14:219 – 22.
 Parker JDA, Bagby RM, Taylor GJ. Alexithymia and depression:
distinct or overlapping constructs? Comp Psychiatry 1991;32:
387 – 94.
 Honkalampi K, Hintikka J, Tanskanen A, Lehtonen J, Viinamaki H.
Depression is strongly associated with alexithymia in the general
population. J Psychosom Res 2000;48:99 – 104.
 Honkalampi K, Saarinen P, Hintikka J, Virtanen V, Viinamaki H.
Factors associated with alexithymia in patients suffering from de-
pression. Psychother Psychosom 1999;68:270 – 5.
 Hendryx MS, Haviland MG, Shaw DG. Dimensions of alexithymia
and their relationship to anxiety and depression. J Pers Assess
1991;56:227 – 37.
 Zeitlin SB, McNally RJ. Alexithymia and anxiety sensitivity in panic
disorder and obsessive – compulsive disorder. Am J Psychiatry 1993;
150:658 – 60.
 Parker JDA, Taylor GJ, Bagby RM, Acklin MW. Alexithymia in
panic disorder and simple phobia: a comparative study. Am J Psy-
chiatry 1993;150:1105– 7.
 Sifneos PE. Alexithymia observations in psychosomatic patients.
Psychother Psychosom 1977;28:47 – 57.
 Taylor GJ, Ryan D, Bagby RM. Toward the development of a new
self-report alexithymia scale. Psychother Psychosom 1985;44:191 – 9.
 Lane RD, Sechrest L, Reidel RG, Weldon V, Kaszniak AW, Schwartz
GE. Impaired verbal and nonverbal emotion recognition in alexithy-
mia. Psychosom Med 1996;58:203 – 10.
 Bermond B. Alexithymie, een neuropsychologische benadering
(Alexithymia, a neuropsychological method of approach). Tijdschr
Psychiatr (J Psychiatry) 1995;37:717– 27.
 Bermond B. Brain and alexithymia. In: Vingerhoets A, van Bussen
F, Boelhouwers J, editors. The (non) expression of emotion in
health and disease. Tilburg, the Netherlands: Tilburg Univ. Press,
1997. pp. 115– 31.
 Taylor GJ, Bagby RM, Parker JDA. The alexithymia construct: a
potential paradigm for psychosomatic medicine. Psychosomatics
1991;32:153 – 63.
 Kirmayer LJ, Robbins JM. Cognitive and social correlates of the
Toronto Alexithymia Scale. Psychosomatics 1993;34:41 – 52.
 Taylor GJ, Bagby RM. Measurement of alexithymia: recommenda-
tions for clinical practice and future research. Psychiatr Clin North
Am 1988;11:351– 64.
 Bagby RM, Parker JDA, Taylor GJ. The twenty-item Toronto Alex-
ithymia Scale: I. Item selection and cross-validation of the factor
structure. J Psychosom Res 1994;38:23 – 32.
 Bagby RM, Taylor GJ, Parker JDA. The twenty-item Toronto Alex-
ithymia Scale: II. Convergent, discriminant and concurrent validity.
J Psychosom Res 1994;38:33 – 40.
 Loas G, Corcos M, Stephan P, Pellet J, Bizouard P, Venisse JL,
Perez-Diaz F, Guelfi JD, Jeammet P. Factorial structure of the 20-
item Toronto Alexithymia Scale Confirmatory factorial analyses in
nonclinical and clinical samples. J Psychosom Res 2001;50:255 – 61.
 Zech E, Luminet O, Rime
´B, Wagner H. Alexithymia and its meas-
urement: confirmatory factor analyses of the 20-item Toronto Alex-
ithymia Scale and the Bermond – Vorst Alexithymia Questionnaire.
Eur J Pers 1999;13:511 – 32.
 Vorst HCM, Bermond B. Validity and reliability of the Bermond–
Vorst Alexithymia Questionnaire. Pers Individ Differ 2001;30:
413 – 34.
 Tucker DM. Lateral brain function, emotion, and conceptualization.
Psychol Bull 1981;89:19 – 46.
 Gainotti G. Disorders of emotions and affect in patients with unilat-
eral brain damage. In: Boller F, Grafman J, editors. Handbook of
neuropsychology, vol. 5. Amsterdam, the Netherlands: Elsevier,
1989. pp. 345 – 58.
 Gazzaniga MS. The organization of the human brain. Science
1989;245:947 – 52.
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541 539
 Kolb B, Whishaw IQ. Fundamentals of human neuropsychology.
3rd ed. New York: Freeman, 1990.
 Joseph R. The right brain and the unconscious: discovering the
stranger within. New York: Plenum, 1992.
 Bear DM. Hemispheric specialization and the neurology of emotion.
Arch Neurol 1983;40:195 – 202.
 Gainotti G, Caltagirone C, Zoccolotti P. Left/right and cortical/sub-
cortical dichotomies in the neuropsychological study of human emo-
tions. Cogn Emot 1993;7:71 – 93.
 Hoppe KD. Hemispheric specialization and creativity. Psychiatr Clin
North Am 1988;11:303 – 15.
 Hoppe KD, Bogen JE. Alexithymia in twelve commissurotomized
patients. Psychother Psychosom 1976;28:148 – 55.
 TenHouten WD, Hoppe KD, Bogen JE, Walter DO. Alexithymia and
the split brain: I. Lexical-level content analysis. Psychother Psycho-
som 1985;43:202 – 8.
 Houtveen JH, Bermond B, Elton MR. Alexithymia: a disruption in a
cortical network? An EEG power and coherence analysis. J Psycho-
physiol 1997;11:147– 57.
 Parker JD, Keightley ML, Smith CT, Taylor GJ. Interhemispheric
transfer deficit in alexithymia: an experimental study. Psychosom
Med 1999;61:464 – 8.
 Parker JDA, Taylor GJ, Bagby RM. Alexithymia and the recognition
of facial expressions of emotion. Psychother Psychosom 1993;59:
197 – 202.
 Jessimer M, Markham R. Alexithymia: a right hemisphere dysfunc-
tion specific to recognition of certain facial expressions? Brain Cogn
1997;34:246 – 58.
 Davidson RJ, Ekman P, Saron C, Senulis J, Friesen WV. Approach/
withdrawal and cerebral asymmetry: emotional expression and brain
physiology. Int J Pers Soc Psychol 1990;58:330 – 41.
 Gazzaniga M, LeDoux JE. The integrated mind. New York: Plenum,
 Buchanan DC, Waterhouse GJ, West S. A proposed neurophysiolog-
ical basis of alexithymia. Psychother Psychosom 1980;34:248 – 55.
 Sperry RW, Zaidel E, Zaidel D. Self recognition and social aware-
ness in the deconnected minor hemisphere. Neuropsychologia
1979;17: 153 – 66.
 TenHouten WD, Hoppe KD, Bogen JE, Walter DO. Alexithymia and
the split brain: II. Sentential-level content analysis. Psychother Psy-
chosomatics 1985;44:1 – 5.
 TenHouten WD, Hoppe KD, Bogen JE, Walter DO. Alexithymia and
the split brain: III. Global-level content analysis of fantasy and sym-
bolization. Psychother Psychosom 1985;44:89 – 94.
 Zeitlin SB, Lane RD, O’Leary DS, Schrift MJ. Interhemispheric
transfer deficit and alexithymia. Am J Psychiatry 1989;146:1434 – 9.
 Geffen G, Nilsson J, Quinn K, Teng EL. The effect of lesions of the
corpus callosum on finger localization. Neuropsychologia 1985;23:
497 – 514.
 Lassonde M, Sauerwein H, McCabe N, Laurencelle L, Geoffry G.
Extent and limits of cerebral adjustment to early section or con-
genital absence of the corpus callosum. Behav Brain Res 1988;30:
165 – 81.
 Dewaraja R, Sasaki Y. A left to right hemisphere callosal transfer
deficit of nonlinguistic information in alexithymia. Psychother Psy-
chosom 1990;54:201 – 7.
 Parker JDA, Taylor GJ, Bagby RM, Thomas S. Problems with meas-
uring alexithymia. Psychosomatics 1991;32:197 – 202.
 TenHouten WD, Hoppe KD, Bogen JE, Walter DO. Alexithymia and
the split brain: V. EEG alpha-band interhemispheric coherence anal-
ysis. Psychother Psychosom 1987;47:1 – 10.
 TenHouten WD, Hoppe KD, Bogen JE, Walter DO. Alexithymia and
the split brain: VI. Electroencephalographic correlates of alexithy-
mia. Psychiatr Clin North Am 1988;11:317 – 29.
 Mandal MK, Borod JC, Asthana HS, Mohanty A, Mohanty S, Koff
E. Effects of lesion variables and emotion type on the perception of
facial emotion. J Nerv Ment Dis 1999;187:603 – 9.
 Cicero BA, Borod JC, Santschi C, Erhan HM, Obler LK, Agosti RM,
Welkowitz J, Grunwald IS. Emotional versus nonemotional lexical
perception in patients with right and left brain damage. Neuropsy-
chiatry Neuropsychol Behav Neurol 1999;12:255 – 64.
 Borod JC, Cicero BA, Obler LK, Welkowitz J, Erhan HM, Santschi
C, Grunwald IS, Agosti RM, Whalen JR. Right hemisphere emo-
tional perception: evidence across multiple channels. Neuropsychol-
ogy 1998;12:446 – 58.
 Borod JC. Perception of facial emotion in schizophrenic and right
brain-damaged patients. J Nerv Ment Dis 1993;181:494 – 502.
 Borod JC, Andelman F, Obler LK, Tweedy JR, Welkowitz J. Right
hemisphere specialization for the identification of emotional words
and sentences: evidence from stroke patients. Neuropsychologia
1992;30:827 – 44.
 Mann LS, Wise TN, Trinidad A, Kohanski R. Alexithymia, affect
recognition, and the five-factor model of personality in normal sub-
jects. Psychol Rep 1994;74:563 – 7.
 Ross ED. Right hemisphere’s role in language, affective behavior
and emotion. Trends Neurosci 1984;7:342 – 6.
 Fricchione G, Howanitz E. Aprosodia and alexithymia: a case report.
Psychother Psychosom 1985;43:156 – 60.
 Parker JDA, Taylor GJ, Bagby RM. Relationship between Conjugate
Lateral Eye Movements and alexithymia. Psychother Psychosom
1992;57:94 – 101.
 Borod JC. Interhemispheric and intrahemispheric control of emotion:
a focus on unilateral brain damage. J Consult Clin Psychol 1992;60:
339 – 48.
 Stuss DT, Gow CA, Hetherington CR. ‘‘No longer Gage’’: frontal
lobe dysfunction and emotional changes. J Consult Clin Psychol
1992;60: 349 – 59.
 McDonald PW, Prkachin KM. The expression and perception of
facial emotion in alexithymia: a pilot study. Psychosom Med
1990;52:199 – 210.
 Kandel EJ, Schwartz JH, Jessel TM. Principles of neural science.
London: Prentice-Hall, 1991.
 Malloy P, Duffy J. The frontal lobes in neuropsychiatric disorders.
In: Boller F, Grafman J, editors. Handbook of neuropsychology, vol.
9. Amsterdam, the Netherlands: Elsevier, 1994. pp. 203 – 32.
 Rolls ET. A theory of emotion and consciousness, and its application
to understanding the neural basis of emotion. In: Gazzaniga MS,
editor. The cognitive neurosciences. Cambridge: MIT Press, 1995.
pp. 1091 – 106.
 Hornak J, Rolls ET, Wade D. Face and voice expression identifica-
tion in patients with emotional and behavioural changes following
ventral frontal lobe damage. Neuropsychologia 1996;34:247 – 61.
 Neafsey EJ. Prefrontal cortical control of the autonomic nervous
system: anatomical and physiological observations. Prog Brain Res
1990;85:147 – 66.
 Damasio AR, van Hoesen GW. Emotional disturbances associated
with focal lesions of the limbic frontal lobe. In: Heilman KM, Satz
SP, editors. Neuropsychology of human emotion. New York: Guil-
ford Press, 1983. pp. 85 – 110.
 Devinsky O, Morrell MJ, Vogt BA. Contributions of anterior cingu-
late cortex to behavior. Brain 1995;118:279 – 306.
 Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz
GE. Neural correlates of levels of emotional awareness: evidence of
an interaction between emotion and attention in the anterior cingulate
cortex. J Cogn Neurosci 1998;104:525 – 35.
 Berthoz S, Artiges E, van de Moortele PF, Poline JB, Rouquette S,
Martinot JL. Emotion-inducing stimuli processing in alexithymia: an
fMRI study (Abstract). Biol Psychiatry 2000;47:110S.
 de Bruin JPC. Social behavior and the prefrontal cortex. Prog Brain
Res 1990;85:485 – 97.
 Alexander GE, Crutcher MD, DeLong MR. Basal ganglia – thalamo-
cortical circuits: parallel substrates for motor, oculomotor, ‘‘prefron-
tal’’ and ‘‘limbic’’ functions. Prog Brain Res 1990;85:119– 47.
 Berman KF, Weinberger DR. The prefrontal cortex in schizophrenia
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541540
and other neuropsychiatric diseases: in vivo physiological correlates
of cognitive deficits. Prog Brain Res 1990;85:521– 37.
 Papckiak AS, Fuerstein M, Spiegel JA. Stress reactivity in alexithy-
mia: decoupling of physiological and cognitive responses. J Hum
Stress 1985;11:135– 42.
 Martin JB, Pihl RO. Influence of alexithymic characteristics on phys-
iological and subjective stress responses in normal individuals. Psy-
chother Psychosom 1986;45:66 – 77.
 Fukunishi I, Sei H, Morita Y, Rahe RH. Sympathetic activity in alex-
ithymics with mother’s low care. J Psychosom Res 1999;46:579– 89.
 Friedlander L, Lumley MA, Farchione T, Doyal G. Testing the alex-
ithymia hypothesis: physiological and subjective responses during
relaxation and stress. J Nerv Ment Dis 1997;185:233 – 9.
 Martin JB, Pihl RD, Pohl RO. Influence of alexithymic character-
istics on physiological and subjective stress responses in normal
individuals. Psychother Psychosom 1986;45:66 – 77.
 Linden W, Lenz JW, Stossel C. Alexithymia, defensiveness and car-
diovascular reactivity to stress. J Psychosom Res 1996;41:575– 83.
 Wehmer F, Brejnak C, Lumley M, Stettner L. Alexithymia and phys-
iological reactivity to emotion-provoking visual scenes. J Nerv Ment
Dis 1995;183:351 – 7.
 Roedema TM, Simons RF. Emotion-processing deficit in alexithy-
mia. Psychophysiology 1999;36:379 – 87.
 Kolb B, Taylor L. Neocortical substrates of emotional behavior. In:
Stein NL, Leventhal B, Trabasso T, editors. Psychological and bio-
logical approaches to emotion. Hillsdale (NJ): Lawrence Erlbaum
Associates, 1990. pp. 115 – 44.
 Heller W. The neuropsychology of emotion: developmental pat-
terns and implications for psychopathology. In: Stein NL, Leventhal
B, Trabasso T, editors. Psychological and biological approaches
to emotion. Hillsdale (NJ): Lawrence Erlbaum Associates, 1990.
pp. 167 – 215.
 Heilman KM, Gilmore RL. Cortical influences in emotion. J Clin
Neurophysiol 1998;15:409 – 23.
 Hellige JB. Hemispheric asymmetry: what’s right and what’s left.
Cambridge: Harvard Univ. Press, 1993.
 Passingham R. The frontal lobes and voluntary action. Oxford: Ox-
ford Univ. Press, 1993.
 Damasio AR, Tranel D, Damasio H. Individuals with sociopathic
behavior caused by frontal damage fail to respond autonomically
to social stimuli. Behav Brain Res 1990;41:81 – 94.
 Henry JP, Haviland MG, Cummings MA, Anderson DL, Nelson JC,
MacMurray JP, et al. Shared neuroendocrine patterns of post-trau-
matic stress disorder and alexithymia. Psychosom Med 1992;54:
407 – 15.
 Dekker C. Psychophysiological responsiveness in recently diagnosed
patients with rheumatoid arthritis. Dordrecht: Utrecht Univ. Press,
 Todarello O, Casamassima A, Daniele S, Marinaccio M, Fanciullo F,
Valentino L, Tedesco N, Wiesel S, Simone G, Marinaccio L. Alex-
ithymia, immunity and cervical intraepithelial neoplasia: replication.
Psychother Psychosom 1997;66:208 – 13.
 Dewaraja R, Tanigawa T, Araki S, Nakata A, Kawamura N, Ago Y,
Sasaki Y. Decreased cytotoxic lymphocyte counts in alexithymia.
Psychother Psychosom 1997;66:83 – 6.
 Bermond B, Vorst CM, Vingerhoets AJM, Gerritsen W. The Amster-
dam alexithymia scale: its psychometric values and correlations with
other personality traits. Psychother Psychosom 1999;68:241 – 51.
 Salminen JK, Saarijarvi S, Aairela E, Tamminen T. Alexithymia:
state or trait? One-year follow-up study of general hospital psychi-
atric consultation outpatients. J Psychosom Res 1994;38:681 – 5.
 Martinez-Sanchez F, Ato-Garcia M, Adam EC, Medina TBH, Espa-
na JS. Stability in alexithymia levels: a longitudinal analysis on
various emotional answers. Pers Individ Differ 1998;24:767 – 72.
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541 541