Cognitive and emotional characteristics of Alexithymia (PDF

Journal of Psychosomatic Research 54 (2003) 533 – 541
Cognitive and emotional characteristics of alexithymia
A review of neurobiological studies
Junilla K. Larsena,*, Nico Branda, Bob Bermondb, Ron Hijmanc
a
Department of Health Psychology, Utrecht University, Postbus 80140, Utrecht 3508 TC, Netherlands
b
Department of Neuropsychology, University of Amsterdam, Amsterdam, Netherlands
c
Department of Psychiatry, University Medical Center of Utrecht, Utrecht, Netherlands
Received 7 November 2001; accepted 29 April 2002
Abstract
Objective: To review neurobiological studies of alexithymia in order to achieve a better understanding of the relationship between alexithymia and psychosomatic diseases and
psychiatric illnesses. Methods: Neurobiological studies of
alexithymia were reviewed with a special focus on how emotional and cognitive elements of alexithymia are reflected in
earlier research. Results: Studies that have correlated alexithymia 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 characteristics 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.
D 2003 Elsevier Inc. All rights reserved.
Keywords: Alexithymia; Neurobiology; Right hemisphere; Commissurotomy; Interhemispheric transfer; Frontal lobe
Introduction
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 [1]. 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
[18] introduced the term ‘alexithymia’ for these emotional
difficulties, which was derived from ‘‘the Greek alexis
(no words), thymos (emotion).’’ Five salient characteristics
* Corresponding author. Tel.: +31-302-533027.
E-mail address: [email protected] (J.K. Larsen).
0022-3999/03/$ – see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0022-3999(02)00466-X
of alexithymia have been described: (1) a reduction or
incapacity to experience emotions; (2) a reduction or incapacity 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 [17], others suggest that the
fundamental deficit in alexithymia is a limited — and in
extreme cases nonexistent — ability to consciously experience emotion [20]. 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 accompanying 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
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alexithymia is useful towards examining the existing literature 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 questionable 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 [1]. For several years, however, the
Toronto Alexithymia Scale (TAS) has proven to be the most
reliable and valid method for measuring several characteristics of alexithymia [23 –25]. The TAS demonstrated a
replicable four-factor structure: difficulty identifying feelings (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 assessing 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) verbalizing 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 subscales emotionalizing and fantasizing representing an emotional component, and the subscales identifying, analyzing
and verbalizing emotions representing a cognitive component 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 [29]. 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.
Research aim
Alexithymia has often been attributed to neurobiological
dysfunctioning. Some studies found evidence for dysfunctioning 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 orbitofrontal cortex. The aim of this article is to review neurobiological studies of alexithymia in order to achieve a
better understanding of the relationship between alexithymia 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 [21].
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 interhemispheric 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 [32]. This model has been further expanded
by Davidson et al. [45], 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
[45]. A third neurobiological hypothesis has been derived
from this model: (C) alexithymia is the result of dysfunctional mechanisms in the frontal cortex. The above-mentioned 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 [46], 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 [21]. The
hypothesized relationship between blockage of corpus cal-
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541
losum functioning and Type II alexithymia has been strengthened through the descriptions of persons with corpus callosum 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 alexithymia. In a preliminary investigation of 12 split-brain individuals, Hoppe and Bogen [39] 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 characteristics of alexithymia, the decreased capacity for fantasy is an
emotional aspect of alexithymia [30]. Thus, these results are
in line with the hypothesis that complete cerebral commissurotomy 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, commissurotomized patients showed a decreased capacity for fantasy and use of symbols (emotional aspects of alexithymia)
and difficulties in describing feelings (cognitive aspect
of alexithymia).
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 alexithymia was provided by studies using a tactile finger localization task to assess the efficiency of interhemispheric
communication [42,51]. This task requires the transfer of
information across the corpus callosum for successful performance, 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
task [52,53].
A study by Zeitlin et al. [51] compared the efficiency of
interhemispheric transfer in 15 alexithymic and 7 nonalexithymic patients suffering from posttraumatic stress disorder
(PTSD) and 10 controls in using the tactile finger localization 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-
535
spheric transfer. Parker et al. [42] 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 [51]. Another explanation is that in the noncommissurotomized alexithymic patients, the disconnection
is less absolute and more functional in nature. In an
extension of the study of Zeitlin et al. [51], Dewaraja and
Sasaki [54] examined the relationship between interhemispheric transfer and alexithymia using both linguistic and
nonlinguistic Japanese symbolic stimuli. Alexithymia was
assessed using the MMPI alexithymia scale and the Schalling Sifneos Personality Scale — Revised (SSPS-R). While
both instruments have proven unsatisfactory psychometric
qualities [55], 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. [51] found
a bidirectional relationship between cognitive aspects of
alexithymia and the callosal transfer process, Dewaraja and
Sasaki [54] found a unidirectional (right-to-left) relationship. The processing of linguistic information is known to
be mainly associated with the left hemisphere, while sensorimotor processing is not known to be associated with a
particular hemisphere. Therefore, the finding of a unidirectional relationship by Dewaraja and Sasaki [54] 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 [41] using the BVAQ. The EEG was continuously 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
interhemispheric transfer.
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 commissurotomized 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,
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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 individuals 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 [64] and Fricchione and Howanitz [65] 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 symptoms 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 alexithymic 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 compared on functioning of the right cerebral hemisphere.
Conjugated lateral eye movements (CLEMs) have sometimes 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. [66], 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 predominance 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 [66].
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 [45].
However, experimental studies of right-brain-damaged and
left-brain-damaged patients show that when the intrahemispheric site of lesion was examined, anterior regions (i.e.,
frontal lobe) were more critical for emotional expression
than posterior regions, independent of valence [67]. Stuss
et al. [68] 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 [69], 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 approximately 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 emotional 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
[72]. 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 emotional experience and related behavior [73]. Electrical
stimulation of the orbitofrontal cortex produces many
autonomic responses [74] and, moreover, orbitofrontal
lesions are associated either with a blunting of emotional
responses, including the attenuation of autonomic accompaniments of emotion, or intense expression of affect with
loss of inhibitions [70]. Emotionally disturbed alexithymic
individuals resemble the blunted rather than the disinhibited 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 [73], merely reflecting cognitive
characteristics of alexithymia.
Since normal subjects’ emotional awareness was associated with greater activation in the ACC during elicitation
of film- and recall-induced emotion [77], it was hypothesized 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 [78]. Intergroup comparisons revealed that alexithymics had higher activation associated with positive pictures, but showed no effect of arousal with negative
J.K. Larsen et al. / Journal of Psychosomatic Research 54 (2003) 533–541
pictures. Main differences were concerned with medial
prefrontal (Brodmann’s area 9) and ACC regions. Although 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. [73]
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 decreases) in the capacity to feel negative or positive
emotions was quite variable across patients. It is possible
that different subregions within the ventromedial prefrontal 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 [80]. Two basal ganglia
neural circuits have been described: the dorsolateral prefrontal circuit and the lateral orbitofrontal circuit (for
detailed descriptions, see Ref. [80]). 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 participates in both circuits [22]. 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 [81]. Overall, depletion of dopamine in the ACC or
the orbitofrontal cortex may produce both cognitive and
emotional characteristics of alexithymia, defined by Bermond [21,22] as Type I alexithymia.
Alexithymia, sympathetic activity, somatic diseases and
psychiatric illnesses
Sympathetic activity
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].
537
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 [1]. Therefore, they will
experience prolonged stress and related physiological hyperarousal, 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 hemisphere [90,91]. Heilman and Gilmore [92] have suggested
that the right hemisphere is more in touch with subcortical
systems that are important for arousal and intention. Moreover, it appears that cerebral arousal is mediated by norepinephrine (NE), which, although widespread, is mainly
supposed to be innervated by right hemispheric pathways
[93]. On the basis of these findings, it may be expected that
alexithymia produced by right hemisphere deficits is associated 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 [74] 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 [22].
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. [96] demonstrating that, although the mean level of
sympathetic activation (as measured by 3-methoxy-4hydroxyphenylethylene glycol levels, MHPG) in alexithymic 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 [74] 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 hemisphere will also result into a reduction of psychosomatic
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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- and badrenergic receptors that have been found on immune cells
and organs [97]. In agreement with this, some research has
found an association between alexithymia and reduced
levels of immunity [98,99]. Dewaraja et al. [99] 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 gastrointestinal disorders and chronic pain [2 –7]. Moreover, several
researchers have explored the relationships between alexithymia 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 depression 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 [51]. Although many studies found
varying correlations between alexithymia and psychiatric
illnesses, no attention has been paid to the fact that
different characteristics of alexithymia could be differentiated. With reference to possible psychiatric complaints,
such a differentiation is important. Although Type I alexithymics do experience a host of problems, they are — due
to the seriously reduced level of emotionalizing — still free
from emotional problems [100], whereas Type II alexithymics do mention such problems. This is understandable
since they do get emotionally aroused, but cannot — due
to the lack of emotion accompanying cognitions — understand the felt emotional arousal, resulting in further emotional problems [1]. 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 various psychiatric illnesses. Prospective studies are needed
for that. From longitudinal studies, it appears that alexithymia is a stable trait, in contrast to functional somatic
symptoms and psychological distress that change over
time [101,102].
Discussion
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
[21,22].
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 unidirectional 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. Moreover, right unilateral cortical lesions often result into emotional 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 accompanying the emotion.
Many studies of patients with frontal lobe damage find a
reduction in emotional expression [68], which has also been
found in alexithymic patients [69]. 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) 533–541
form) by the absence of the emotional experience and,
consequently, by the absence of the cognition accompanying 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. Without 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 nonalexithymic 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.
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